Difference between revisions of "Talk:2014 Group 1 Project"

From CellBiology
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and z3420257 research: flotillin-dependent endocytosis and macropinocytosis
 
and z3420257 research: flotillin-dependent endocytosis and macropinocytosis
  
and z3375490 research: circular doral ruffles and phagocytosis
+
and z3375490 research: circular dorsal ruffles and phagocytosis
  
 
and z3399239 research: trans-endocytosis and endocytosis in general
 
and z3399239 research: trans-endocytosis and endocytosis in general
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The article ‘Integrins traffic rapidly via circular dorsal ruffles and macropinocytosis during stimulated cell migration’ presents that upon cell stimulation with platelet derived growth factor do not undergo significant endocytosis at ventral focal adhesions.  Instead, it is redistributed to dorsal circular ruffles. This was assessed using 4-D confocal live-cell imaging.  Additionally, integrins transit through recycling endosomal compartments to repopulate new focal adhesion on the ventral surface.
 
The article ‘Integrins traffic rapidly via circular dorsal ruffles and macropinocytosis during stimulated cell migration’ presents that upon cell stimulation with platelet derived growth factor do not undergo significant endocytosis at ventral focal adhesions.  Instead, it is redistributed to dorsal circular ruffles. This was assessed using 4-D confocal live-cell imaging.  Additionally, integrins transit through recycling endosomal compartments to repopulate new focal adhesion on the ventral surface.
  
====Reference====
+
Reference
 +
 
 
<pubmed>21464228</pubmed>| [http://www.ncbi.nlm.nih.gov/pubmed/21464228 Pubmed]
 
<pubmed>21464228</pubmed>| [http://www.ncbi.nlm.nih.gov/pubmed/21464228 Pubmed]
  
===Copyright===
+
Copyright
 
@2013 Zhizhan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 
@2013 Zhizhan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
  
Line 144: Line 145:
 
The article ‘Contemporaneous cell spreading and phagocytosis: Magneto-resistive real-time monitoring of membrane competing processes’ by Shoshi et al investigate that during phagocytosis the cell membrane expands, to engulf particles (in this case beads on surfaces), by cell spreading.  The engulfment rate was additionally measured using real-time magneto-resistive monitoring, with an average of 3 beads per minute. Correspondingly, the rate of engulfment was not a linear function but is high at an early stage, then decreases steadily until saturation.  
 
The article ‘Contemporaneous cell spreading and phagocytosis: Magneto-resistive real-time monitoring of membrane competing processes’ by Shoshi et al investigate that during phagocytosis the cell membrane expands, to engulf particles (in this case beads on surfaces), by cell spreading.  The engulfment rate was additionally measured using real-time magneto-resistive monitoring, with an average of 3 beads per minute. Correspondingly, the rate of engulfment was not a linear function but is high at an early stage, then decreases steadily until saturation.  
  
===Reference===
+
Reference
 
<pubmed>22770907</pubmed>| [http://www.ncbi.nlm.nih.gov/pubmed/22770907 Pubmed]
 
<pubmed>22770907</pubmed>| [http://www.ncbi.nlm.nih.gov/pubmed/22770907 Pubmed]
  
Line 226: Line 227:
 
The article ‘Integrins traffic rapidly via circular dorsal ruffles and macropinocytosis during stimulated cell migration’ presents that upon cell stimulation with platelet derived growth factor do not undergo significant endocytosis at ventral focal adhesions.  Instead, it is redistributed to dorsal circular ruffles. This was assessed using 4-D confocal live-cell imaging.  Additionally, integrins transit through recycling endosomal compartments to repopulate new focal adhesion on the ventral surface.
 
The article ‘Integrins traffic rapidly via circular dorsal ruffles and macropinocytosis during stimulated cell migration’ presents that upon cell stimulation with platelet derived growth factor do not undergo significant endocytosis at ventral focal adhesions.  Instead, it is redistributed to dorsal circular ruffles. This was assessed using 4-D confocal live-cell imaging.  Additionally, integrins transit through recycling endosomal compartments to repopulate new focal adhesion on the ventral surface.
  
====Reference====
+
Reference
 
<pubmed>21464228</pubmed>| [http://www.ncbi.nlm.nih.gov/pubmed/21464228 Pubmed]
 
<pubmed>21464228</pubmed>| [http://www.ncbi.nlm.nih.gov/pubmed/21464228 Pubmed]
  
===Copyright===
+
Copyright
 
@2013 Zhizhan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 
@2013 Zhizhan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
  
Line 235: Line 236:
 
macropinocytosis during stimulated cell migration'  Zhizhan Gu, Erika H. Noss, Victor W. Hsu, and Michael B. Brenner, (2011) The Journal of Cell Biology 2011 Apr 4;193(1):61-70. doi: 10.1083/jcb.201007003
 
macropinocytosis during stimulated cell migration'  Zhizhan Gu, Erika H. Noss, Victor W. Hsu, and Michael B. Brenner, (2011) The Journal of Cell Biology 2011 Apr 4;193(1):61-70. doi: 10.1083/jcb.201007003
  
===phagocytosis===
+
====phagocytosis====
  
 
The article ‘Contemporaneous cell spreading and phagocytosis: Magneto-resistive real-time monitoring of membrane competing processes’ by Shoshi et al investigate that during phagocytosis the cell membrane expands, to engulf particles (in this case beads on surfaces), by cell spreading.  The engulfment rate was additionally measured using real-time magneto-resistive monitoring, with an average of 3 beads per minute. Correspondingly, the rate of engulfment was not a linear function but is high at an early stage, then decreases steadily until saturation.  
 
The article ‘Contemporaneous cell spreading and phagocytosis: Magneto-resistive real-time monitoring of membrane competing processes’ by Shoshi et al investigate that during phagocytosis the cell membrane expands, to engulf particles (in this case beads on surfaces), by cell spreading.  The engulfment rate was additionally measured using real-time magneto-resistive monitoring, with an average of 3 beads per minute. Correspondingly, the rate of engulfment was not a linear function but is high at an early stage, then decreases steadily until saturation.  
  
===Reference===
+
Reference
 
<pubmed>22770907</pubmed>| [http://www.ncbi.nlm.nih.gov/pubmed/22770907 Pubmed]
 
<pubmed>22770907</pubmed>| [http://www.ncbi.nlm.nih.gov/pubmed/22770907 Pubmed]
  
===Copyright===
+
Copyright
 
@2012 Shoshi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 
@2012 Shoshi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
  
Line 251: Line 252:
 
Membrane during Phagocytosis’ journal, by Shim et al, put forward that a Rab GTPases, called Rab35, regulate trafficking from the cell membrane to the cytoplasm. Rab35 is a specific regulator of the actin cytoskeleton in the plasma membrane and play a role in filopodia and lamellipodia. In addition, Rab35 is essential for Cdc42 and Rac1 localization at an activated plasma membrane, when in contact with foreign particles and therefore is crucial for actin rearrangement during phagocytosis. Drosophilas were used to demonstrate the hypothesis and presence/absence of Rab35 effecting phagocytosis.
 
Membrane during Phagocytosis’ journal, by Shim et al, put forward that a Rab GTPases, called Rab35, regulate trafficking from the cell membrane to the cytoplasm. Rab35 is a specific regulator of the actin cytoskeleton in the plasma membrane and play a role in filopodia and lamellipodia. In addition, Rab35 is essential for Cdc42 and Rac1 localization at an activated plasma membrane, when in contact with foreign particles and therefore is crucial for actin rearrangement during phagocytosis. Drosophilas were used to demonstrate the hypothesis and presence/absence of Rab35 effecting phagocytosis.
  
===Reference===
+
Reference
 
<pubmed>20065041</pubmed>| [http://www.ncbi.nlm.nih.gov/pubmed/20065041 Pubmed]
 
<pubmed>20065041</pubmed>| [http://www.ncbi.nlm.nih.gov/pubmed/20065041 Pubmed]
  
===Copyright===
+
Copyright
 
@2010 Shim et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 
@2010 Shim et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
  
Line 262: Line 263:
 
The article ‘Plasma membrane tension orchestrates membrane trafficking, cytoskeletal remodeling, and biochemical signaling during phagocytosis’ focus on the 2 phases of pseudopod extension that included actin polymerization pushing the membrane forward and increased membrane tension using high-resolution microscopy of macrophages attempting to internalize an IgG-opsonized glass surface. A 50% increase in tether force was observed in phagocytic cells, compared to the resting cells membrane tension. Additionally, inward bead movement (engulfment) and ingestion is most probably due to contraction and exocytosis activation. This confirms that membrane tension is an exocytosis activator and that exocytosis is required for phagocytosis to complete.
 
The article ‘Plasma membrane tension orchestrates membrane trafficking, cytoskeletal remodeling, and biochemical signaling during phagocytosis’ focus on the 2 phases of pseudopod extension that included actin polymerization pushing the membrane forward and increased membrane tension using high-resolution microscopy of macrophages attempting to internalize an IgG-opsonized glass surface. A 50% increase in tether force was observed in phagocytic cells, compared to the resting cells membrane tension. Additionally, inward bead movement (engulfment) and ingestion is most probably due to contraction and exocytosis activation. This confirms that membrane tension is an exocytosis activator and that exocytosis is required for phagocytosis to complete.
  
===Reference===
+
Reference
 
<pubmed>23821745</pubmed>| [http://www.ncbi.nlm.nih.gov/pubmed/23821745 Pubmed]
 
<pubmed>23821745</pubmed>| [http://www.ncbi.nlm.nih.gov/pubmed/23821745 Pubmed]
  
===Copyright===
+
Copyright
 
@2013 Masters et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 
@2013 Masters et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
  
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[[http://php.med.unsw.edu.au/cellbiology/index.php?title=File:Pnas.1301766110fig01.jpg#Reference]]
 
[[http://php.med.unsw.edu.au/cellbiology/index.php?title=File:Pnas.1301766110fig01.jpg#Reference]]
  
 +
[[File:Pnas.1301766110fig01.jpg]
  
 
--[[User:Z3420257|Z3420257]] ([[User talk:Z3420257|talk]]) 22:24, 1 April 2014 (EST)
 
--[[User:Z3420257|Z3420257]] ([[User talk:Z3420257|talk]]) 22:24, 1 April 2014 (EST)

Revision as of 21:22, 3 April 2014

2014 Projects: Group 1 | Group 2 | Group 3 | Group 4

  1. Do not remove this notice {{2014 Project discussion}} from the top of the discussion page.
  2. Newest student comments should be entered at the top of this current page under the subheading "Student Discussion Area" (you cannot edit the sub-heading title).
  3. All comments should begin with your own signature button, that will automatically enter student number date/time stamp.
  4. Do not use your full name here in discussion, if absolutely necessary you may use first names only.
  5. Do not remove or edit other student comments.
  6. Use sub-headings if you want to add other draft information, images, references, etc.
  7. Only your own group members should edit this page, unless directed otherwise by the course co-ordinator.

Group Assessment Criteria

  1. The key points relating to the topic that your group allocated are clearly described.
  2. The choice of content, headings and sub-headings, diagrams, tables, graphs show a good understanding of the topic area.
  3. Content is correctly cited and referenced.
  4. The wiki has an element of teaching at a peer level using the student's own innovative diagrams, tables or figures and/or using interesting examples or explanations.
  5. Evidence of significant research relating to basic and applied sciences that goes beyond the formal teaching activities.
  6. Relates the topic and content of the Wiki entry to learning aims of cell biology.
  7. Clearly reflects on editing/feedback from group peers and articulates how the Wiki could be improved (or not) based on peer comments/feedback. Demonstrates an ability to review own work when criticised in an open edited wiki format. Reflects on what was learned from the process of editing a peer's wiki.
  8. Evaluates own performance and that of group peers to give a rounded summary of this wiki process in terms of group effort and achievement.
  9. The content of the wiki should demonstrate to the reader that your group has researched adequately on this topic and covered the key areas necessary to inform your peers in their learning.
  10. Develops and edits the wiki entries in accordance with the above guidelines.


Contents

17 April 2014

Before the next practical class (after the mid-semester break) the following items must be completed:

  1. You have written draft text in the section(s) that you have been assigned by your group.
  2. Your text should include source references clearly identifying original research from review articles.
  3. Your section(s) must include at least one research/review image or student drawn image related to the section topic.
  4. You have clearly identified the work you have contributed on the project discussion page.

Projects will be presented by your group to the rest of the class at the beginning of the next practical.


--Mark Hill (talk) 16:49, 20 March 2014 (EST) --Z3399239 (talk) 16:49, 20 March 2014 (EST) --Z3420257 (talk) 16:49, 20 March 2014 (EST) --Z3373930 (talk) 16:50, 20 March 2014 (EST)

Hello dear colleagues. Is anyone else interested in doing "into the cell from the plasma membrane (Endocytosis)"? --Z3399239 (talk) 16:52, 20 March 2014 (EST)

And if not Endocytosis would anyone be interested in doing "from the trans Golgi network to the cell exterior (Exocytosis) "? --Z3399239 (talk) 12:58, 27 March 2014 (EST)

So would z3373930 research: CLIC/GEEC endocytic pathway and arf6-dependent endocytosis

and z3420257 research: flotillin-dependent endocytosis and macropinocytosis

and z3375490 research: circular dorsal ruffles and phagocytosis

and z3399239 research: trans-endocytosis and endocytosis in general --Z3399239 (talk) 16:58, 27 March 2014 (EST)

Good afternoon fair lads and lasses. I started my research into the two pathways given to me by attempting to gauge an understanding of them which would improve my success in finding related articles. Trouble is, I can't find any clear descriptions of my types of endocytosis?!? All I can gather is that the CLIC / GEEC pathway has something to do with the protein clathrin and the clathrin vesicles (I'm sure by now you have come across these in your research as well - seems to cover most types of endocytosis). Anyway, thought I'd give u the heads up! I will continue to look for articles but they may not be as direct towards my subtypes as I would have liked. We can discuss more in person tomorrow. Peace out. --Z3373930 (talk) 15:46, 2 April 2014 (EST)


--Z3420257 (talk) 14:23, 3 April 2014 (EST)

Hi guys, a few short notes on Macropinocytosis and the Flotillin-linked pathway. The former was easy to research and there are a lot of articles featuring the topic. Most of them talked about the role of actin filaments in this pathway. On the other hand, there was barely any detailed studies on the flotillin-linked pathway. Instead, I included a study involving Clathrin. I think this might be an interesting one as there are a lot of research articles discussing its pathway.

Journal Summaries

Cellular Entry of Ebola Virus Involves Uptake by a Macropinocytosis-Like Mechanism and Subsequent Trafficking through Early and Late Endosomes

<pubmed>20862315</pubmed> | PLoS One

Zaire ebolavirus (ZEBOV) is studied in this publication as it posts a threat to the general public. The study mentions different methods sited previously on how the virus infects the host cell. In this particular study, Saeed et. al has established micropinocytosis as the pathway involved. The paper goes through the factors present in the pathway such as the requirement of free membrane cholesterol (lipid rafts), and the role actin filaments play in macropinosome formation, which involves a ruffle filament folding back on itself, creating a large cavity referred to as a macropinosome.

Human Cytomegalovirus Entry into Dendritic Cells Occurs via a Macropinocytosis-Like Pathway in a pH-Independent and Cholesterol-Dependent Manner

<pubmed>22496863</pubmed> | PLoS One

Supporting the findings of the study conducted by Saeed et.al, this study also demonstrates the ability of cells to engulf materials via macropinocytosis. The involvement of actin filaments was demonstrated by incorporating cytoskeleton pharmacological inhibitors, resulting in the absence of macropinocytosis. Macropinocytosis is generally observed in larger viruses rather than small ones, which have been found to enter the cell via a different form of endocytosis. As demonstrated by both articles, macropinocytosis is a good area of study as it is involved in many disease pathways, especially those of a viral nature.

The Role of Flotillins in Regulating Aβ Production, Investigated Using Flotillin 1-/-, Flotillin 2-/- Double Knockout Mice

<pubmed>24465508</pubmed> | PLoS One

Flotillins are involved in many cell functions such as cell adhesion, signalling, cell membrane interactions and endocytosis. They generally function as adhesion proteins allowing for many cell interactions to occur. Its absence is seen to have an overall negative effect on endocytosis. While this study is not solely concentrated on flotillin’s involvement in endocytosis, it’s relevance lies in the demonstration of its role in cell-cell adhesion.

Although extensive research was conducted on this topic, there is a minimal number of sources covering the role of Flotillin in endocytosis. Any study found to have done so has seen to have lacked in depth analysis of the role it plays in endocytosis. Thus, it can be said that this topic is a good research option for future interests on endocytosis.

Roles of AP-2 in Clathrin-Mediated Endocytosis

<pubmed>20485680</pubmed> | PLoS One

Many studies on endocytosis demonstrate the role of clathrin and the resulting clathrin coated vesicles. This particular study demonstrates the role of the heterotetrameric chalthrin adaptor complex, which is needed for the occurrence of clathrin-related endocytosis. This study focuses on how LDL’s enter the cell via this specific pathway. The absence of AP-2 is suggested to hinder the process of endocytosis in this instance. It is, in conclusion, a very important component of the clathrin-based endocytic pathway. Although not specific to macropinocytosis, this study is able to demonstrate that there is present a number of endocytic pathways involving different proteins.


--Z3399239 (talk) 14:51, 3 April 2014 (EST)

Trans-endocytosis of CD47 and SHPS-1 and its role in regulation of the CD47–SHPS-1 system

<pubmed>18349073</pubmed> This article looks at trans-endocytosis of transmembrane proteins CD47 and SHPS-1. The study suggests that CD47 and SHPS-1 interaction initiates the transfer of CD47 from CD47-expressing cells to neighboring SHPS-1-expressing cells followed by the internalization of the ligand-receptor complex into the SHPS-1-expressing cells. SHPS-1 was found to undergo trans-endocytosis from SHPS-1-expressing cells to neighboring CD47-expressing cells, suggesting that trans-endocytosis of CD47 and SHPS-1 occurs bidirectionally. The study suggests that CD47 trans-endocytosis is implicated in the regulation of the CD47–SHPS-1 system.

This article is relevant to the sub-topic of trans-endocytosis as it describes the mechanism and physiological roles of endocytosis and gives a specific example of trans membrane protein trans-endocytosis.


Trans-Endocytosis of CD80 and CD86: A Molecular Basis for the Cell-Extrinsic Function of CTLA-4

<pubmed>21474713</pubmed>

Qureshi et al. (2011) investigate the cell-extrinsic mechanisms of Cytotoxic T lymphocyte antigen 4 (CTLA-4). CTLA-4 is thought to be an important factor in the prevention of autoimmune disease. Trans-endocytosis of CD80 and CD86 (ligands shared by both CLTA-4 and CD28, a stimulatory receptor) inhibits co-stimulation of CD28. The study suggests trans-endocytosis as a possible cell-extrinsic model of CLTA-4 function whereby co-stimulatory ligands are removed from antigen presenting cells (APCs).

This study is relevant as it outlines a mechanism whereby trans-endocytosis is used to inhibit co-stimulation of another cell. The study also shows that trans-endocytosis can play a regulatory role in autoimmune diseases.


β-Arrestin1 Mediates the Endocytosis and Functions of Macrophage Migration Inhibitory Factor

<pubmed>PMC3026819</pubmed>

Xie et al. (2011) investigate the effects of Macrophage migration inhibitory factor (MIF) and β-Arrestin on MIF endocytosis. The study suggests that MIF utilises β-arrestin1 as a molecular scaffold to maintain integrity and specificity of signalling.

This study relates endocytosis to cytokines and chemical mediators involved regulating inflammatory and immune responses.


Jak2 is a negative regulator of ubiquitin-dependent endocytosis of the growth hormone receptor

<pubmed>21347402</pubmed>

Putters et al. (2011) investigate the ability of Janus kinase 2 (Jak2) to bind to the growth hormone receptor, preventing endocytosis of growth hormone receptor (GHR). The article shows that Jak2 specifically inhibits GHR endocytosis independent of its kinase activity and Growth Hormone-induced and constitutive endocytosis undergo the same mechanism of endocytosis.

This article is relevant because it shows that both growth hormone-induced and constitutive growth hormone receptor endocytosis depend on the same factors, therefore strongly suggesting that the modes of endocytosis are similar, if not identical.


CLIC/GEEC endocytic pathway

Clathrin- and Dynamin-Independent Endocytosis of FGFR3 – Implications for Signalling

<pubmed>21779335</pubmed>

This article confirmed that the best studied endocytic mechanism is characterised by the formation of clarithin (a protein) coated pits at the plasma membrane. Epidermal Growth Factor Receptors (EGFR’s) that were internalised via a clarithin-mediated pathway were found to recycle back to the cell surface whereas EGFR’s that were internalised via a clarithin-independant pathway were degraded. This concluded that different endocytic pathways dictate further signalling and intracellular trafficking of their cargo.

The article is relevant because it categorised the CLIC/GEEC pathway as a clarithin-independant endocytic pathway. The article raised my awareness of the lack of information on this specific pathway. Even though many derivatives of clarithin-inependant endocytosis have been established, they are yet to be given definitive features in order to be repeatedly categorised. Therefore, further research into the subtypes of clarithin-independant pathways may prove difficult.

E3 ubiquitin ligase Pub1 is implicated in endocytosis of a GPI-anchored protein Ecm33 in fission yeast.

<pubmed>24454826</pubmed>

This study demonstrated that a GPI-anchored protein, Ecm33 is endocytosed in a Pub-1 dependant manner that is also required for the trafficking of non-GPI-anchored proteins in fission yeast. Ecm33 is important for cell wall integrity and function. Ubiquitylation was also studied but results were inconclusive in determining whether it is required for internalisation of GPI-anchored proteins. It was found however that when GPI-anchored proteins were endocytosed the main fraction of them were delivered to GEEC’s.

This article was of relevance because it defined GEEC as the acronym for GPI-anchored enriched endosomal compartment. This pathway seems to be specific for a type of protein on the cell membrane surface. Due to the similarities amongst yeast and mammalian cells, this study also provides a basis for further research into understanding the precise mechanism of endocytosis of GPI-anchored proteins in higher eukaryotes.

arf6-dependent endocytosis

Endocytosis of hERG Is Clathrin-Independent and Involves Arf6

<pubmed>24392021</pubmed>

hERG potassium channels are important for repolarisation of the cardiac action potential. Reduced levels of expression increases the risk of ventricular arrhytmias. The results of this study found that this channel undergoes rapid internalisation which is neither inhibited by dynamin (an inhibitor of dynasore) nor Rab5a. This suggests the endocytosis of hERG is a clarithin-independant mechanism. A GTPase deficient mutant, Arf6-Q67L was compared and contrasted on two types of cells, HeLa and H9c2. Both of these had hERG channels present on the characteristic vacuole, concluding that Arf-6 is required for endocytosis of hERG potassium channels.

This article is relevant to the subtype of Arf-6 dependant endocytosis because it explores the clinical significance when this subtype is potentially malfunctioning. It demonstrates how different cells use different signalling mechanisms for endocytosis and how this variation can effect organs at the multicellular level.

ARF6-Dependent Regulation of P2Y Receptor Traffic and Function in Human Platelets

<pubmed>22916275</pubmed>

Arf-6 proteins were found to regulate intracellular trafficking by shuffling between an active GTP-bound form and an inactive GDP-bound form. A low level of Arf-6 GTP is essential for platelet aggregation and this was deduced to be regulated depending on platelet activation by collagen. when platelets are activated, the GTP-bound form of Arf-6 rapidly converts to its GDP-bound form. Arf-6 activity was also found to be stimulated by activation of P2Y purinoreceptors. These findings deduced that Arf-6 is a regulator of platelet function by demonstrating it has a function in internalisation of P2Y purinreceptors which in turn have an effect on platelet ADP receptor function.

This article shed some light on the Arf-6 dependant pathway of endocytosis. It is clear that Arf-6 is a type of kinase signal, controlling the level of endocytosis. Seeing as this endocytic pathway is common in human platelets, it may have close associations in haemolytic pathology and this may be an interesting avenue to investigate as part of the project.

--Z3373930 (talk) 15:11, 3 April 2014 (EST)


circular dosral ruffles

The article ‘Integrins traffic rapidly via circular dorsal ruffles and macropinocytosis during stimulated cell migration’ presents that upon cell stimulation with platelet derived growth factor do not undergo significant endocytosis at ventral focal adhesions. Instead, it is redistributed to dorsal circular ruffles. This was assessed using 4-D confocal live-cell imaging. Additionally, integrins transit through recycling endosomal compartments to repopulate new focal adhesion on the ventral surface.

Reference

<pubmed>21464228</pubmed>| Pubmed

Copyright @2013 Zhizhan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation: ‘Integrins traffic rapidly via circular dorsal ruffles and macropinocytosis during stimulated cell migration' Zhizhan Gu, Erika H. Noss, Victor W. Hsu, and Michael B. Brenner, (2011) The Journal of Cell Biology 2011 Apr 4;193(1):61-70. doi: 10.1083/jcb.201007003

phagocytosis

The article ‘Contemporaneous cell spreading and phagocytosis: Magneto-resistive real-time monitoring of membrane competing processes’ by Shoshi et al investigate that during phagocytosis the cell membrane expands, to engulf particles (in this case beads on surfaces), by cell spreading. The engulfment rate was additionally measured using real-time magneto-resistive monitoring, with an average of 3 beads per minute. Correspondingly, the rate of engulfment was not a linear function but is high at an early stage, then decreases steadily until saturation.

Reference <pubmed>22770907</pubmed>| Pubmed

Copyright @2012 Shoshi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation: '‘Contemporaneous cell spreading and phagocytosis: Magneto-resistive real-time monitoring of membrane competing processes’ A. Shoshi, J.Schotter, P.Schroeder, M.Milnera, P.Ertl, R.Heer, G.Reiss, H.Brueckl (2012) Biosensors andBioelectronics40(2013)82–88. doi: 10.1016/j.bios.2012.06.028. Epub 2012 Jun 23.


‘Rab35 Mediates Transport of Cdc42 and Rac1 to the Plasma Membrane during Phagocytosis’ journal, by Shim et al, put forward that a Rab GTPases, called Rab35, regulate trafficking from the cell membrane to the cytoplasm. Rab35 is a specific regulator of the actin cytoskeleton in the plasma membrane and play a role in filopodia and lamellipodia. In addition, Rab35 is essential for Cdc42 and Rac1 localization at an activated plasma membrane, when in contact with foreign particles and therefore is crucial for actin rearrangement during phagocytosis. Drosophilas were used to demonstrate the hypothesis and presence/absence of Rab35 effecting phagocytosis.

Reference <pubmed>20065041</pubmed>| Pubmed

Copyright @2010 Shim et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation: ‘Rab35 Mediates Transport of Cdc42 and Rac1 to the Plasma Membrane during Phagocytosis' Jaewon Shim, Sun-Min Lee, Myeong Sup Lee, Joonsun Yoon, Hee-Seok Kweon, and Young-Joon Kim (2010) Mol Cell Biol. 2010 Mar;30(6):1421-33. doi: 10.1128/MCB.01463-09. Epub 2010 Jan 11.


The article ‘Plasma membrane tension orchestrates membrane trafficking, cytoskeletal remodeling, and biochemical signaling during phagocytosis’ focus on the 2 phases of pseudopod extension that included actin polymerization pushing the membrane forward and increased membrane tension using high-resolution microscopy of macrophages attempting to internalize an IgG-opsonized glass surface. A 50% increase in tether force was observed in phagocytic cells, compared to the resting cells membrane tension. Additionally, inward bead movement (engulfment) and ingestion is most probably due to contraction and exocytosis activation. This confirms that membrane tension is an exocytosis activator and that exocytosis is required for phagocytosis to complete.

Reference <pubmed>23821745</pubmed>| Pubmed

Copyright @2013 Masters et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation: ‘Plasma membrane tension orchestrates membrane trafficking, cytoskeletal remodeling, and biochemical signaling during phagocytosis' Thomas A. Masters, Bruno Pontes, Virgile Viasnoffa, You Li, and Nils . Gauthier, (2013) Proc Natl Acad Sci U S A. 2013 Jul 16;110(29):11875-80. doi: 10.1073/pnas.1301766110. Epub 2013 Jul 2.


Images

[[1]]


CLIC/GEEC endocytic pathway

Clathrin- and Dynamin-Independent Endocytosis of FGFR3 – Implications for Signalling

<pubmed>21779335</pubmed>

This article confirmed that the best studied endocytic mechanism is characterised by the formation of clarithin (a protein) coated pits at the plasma membrane. Epidermal Growth Factor Receptors (EGFR’s) that were internalised via a clarithin-mediated pathway were found to recycle back to the cell surface whereas EGFR’s that were internalised via a clarithin-independant pathway were degraded. This concluded that different endocytic pathways dictate further signalling and intracellular trafficking of their cargo.

The article is relevant because it categorised the CLIC/GEEC pathway as a clarithin-independant endocytic pathway. The article raised my awareness of the lack of information on this specific pathway. Even though many derivatives of clarithin-inependant endocytosis have been established, they are yet to be given definitive features in order to be repeatedly categorised. Therefore, further research into the subtypes of clarithin-independant pathways may prove difficult.

E3 ubiquitin ligase Pub1 is implicated in endocytosis of a GPI-anchored protein Ecm33 in fission yeast.

<pubmed>24454826</pubmed>

This study demonstrated that a GPI-anchored protein, Ecm33 is endocytosed in a Pub-1 dependant manner that is also required for the trafficking of non-GPI-anchored proteins in fission yeast. Ecm33 is important for cell wall integrity and function. Ubiquitylation was also studied but results were inconclusive in determining whether it is required for internalisation of GPI-anchored proteins. It was found however that when GPI-anchored proteins were endocytosed the main fraction of them were delivered to GEEC’s.

This article was of relevance because it defined GEEC as the acronym for GPI-anchored enriched endosomal compartment. This pathway seems to be specific for a type of protein on the cell membrane surface. Due to the similarities amongst yeast and mammalian cells, this study also provides a basis for further research into understanding the precise mechanism of endocytosis of GPI-anchored proteins in higher eukaryotes.

arf6-dependent endocytosis

Endocytosis of hERG Is Clathrin-Independent and Involves Arf6

<pubmed>24392021</pubmed>

hERG potassium channels are important for repolarisation of the cardiac action potential. Reduced levels of expression increases the risk of ventricular arrhytmias. The results of this study found that this channel undergoes rapid internalisation which is neither inhibited by dynamin (an inhibitor of dynasore) nor Rab5a. This suggests the endocytosis of hERG is a clarithin-independant mechanism. A GTPase deficient mutant, Arf6-Q67L was compared and contrasted on two types of cells, HeLa and H9c2. Both of these had hERG channels present on the characteristic vacuole, concluding that Arf-6 is required for endocytosis of hERG potassium channels.

This article is relevant to the subtype of Arf-6 dependant endocytosis because it explores the clinical significance when this subtype is potentially malfunctioning. It demonstrates how different cells use different signalling mechanisms for endocytosis and how this variation can effect organs at the multicellular level.

ARF6-Dependent Regulation of P2Y Receptor Traffic and Function in Human Platelets

<pubmed>22916275</pubmed>

Arf-6 proteins were found to regulate intracellular trafficking by shuffling between an active GTP-bound form and an inactive GDP-bound form. A low level of Arf-6 GTP is essential for platelet aggregation and this was deduced to be regulated depending on platelet activation by collagen. when platelets are activated, the GTP-bound form of Arf-6 rapidly converts to its GDP-bound form. Arf-6 activity was also found to be stimulated by activation of P2Y purinoreceptors. These findings deduced that Arf-6 is a regulator of platelet function by demonstrating it has a function in internalisation of P2Y purinreceptors which in turn have an effect on platelet ADP receptor function.

This article shed some light on the Arf-6 dependant pathway of endocytosis. It is clear that Arf-6 is a type of kinase signal, controlling the level of endocytosis. Seeing as this endocytic pathway is common in human platelets, it may have close associations in haemolytic pathology and this may be an interesting avenue to investigate as part of the project.

flotillin-dependent endocytosis

macropinocytosis

circular dosral ruffles

The article ‘Integrins traffic rapidly via circular dorsal ruffles and macropinocytosis during stimulated cell migration’ presents that upon cell stimulation with platelet derived growth factor do not undergo significant endocytosis at ventral focal adhesions. Instead, it is redistributed to dorsal circular ruffles. This was assessed using 4-D confocal live-cell imaging. Additionally, integrins transit through recycling endosomal compartments to repopulate new focal adhesion on the ventral surface.

Reference <pubmed>21464228</pubmed>| Pubmed

Copyright @2013 Zhizhan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation: ‘Integrins traffic rapidly via circular dorsal ruffles and macropinocytosis during stimulated cell migration' Zhizhan Gu, Erika H. Noss, Victor W. Hsu, and Michael B. Brenner, (2011) The Journal of Cell Biology 2011 Apr 4;193(1):61-70. doi: 10.1083/jcb.201007003

phagocytosis

The article ‘Contemporaneous cell spreading and phagocytosis: Magneto-resistive real-time monitoring of membrane competing processes’ by Shoshi et al investigate that during phagocytosis the cell membrane expands, to engulf particles (in this case beads on surfaces), by cell spreading. The engulfment rate was additionally measured using real-time magneto-resistive monitoring, with an average of 3 beads per minute. Correspondingly, the rate of engulfment was not a linear function but is high at an early stage, then decreases steadily until saturation.

Reference <pubmed>22770907</pubmed>| Pubmed

Copyright @2012 Shoshi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation: '‘Contemporaneous cell spreading and phagocytosis: Magneto-resistive real-time monitoring of membrane competing processes’ A. Shoshi, J.Schotter, P.Schroeder, M.Milnera, P.Ertl, R.Heer, G.Reiss, H.Brueckl (2012) Biosensors andBioelectronics40(2013)82–88. doi: 10.1016/j.bios.2012.06.028. Epub 2012 Jun 23.


‘Rab35 Mediates Transport of Cdc42 and Rac1 to the Plasma Membrane during Phagocytosis’ journal, by Shim et al, put forward that a Rab GTPases, called Rab35, regulate trafficking from the cell membrane to the cytoplasm. Rab35 is a specific regulator of the actin cytoskeleton in the plasma membrane and play a role in filopodia and lamellipodia. In addition, Rab35 is essential for Cdc42 and Rac1 localization at an activated plasma membrane, when in contact with foreign particles and therefore is crucial for actin rearrangement during phagocytosis. Drosophilas were used to demonstrate the hypothesis and presence/absence of Rab35 effecting phagocytosis.

Reference <pubmed>20065041</pubmed>| Pubmed

Copyright @2010 Shim et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation: ‘Rab35 Mediates Transport of Cdc42 and Rac1 to the Plasma Membrane during Phagocytosis' Jaewon Shim, Sun-Min Lee, Myeong Sup Lee, Joonsun Yoon, Hee-Seok Kweon, and Young-Joon Kim (2010) Mol Cell Biol. 2010 Mar;30(6):1421-33. doi: 10.1128/MCB.01463-09. Epub 2010 Jan 11.


The article ‘Plasma membrane tension orchestrates membrane trafficking, cytoskeletal remodeling, and biochemical signaling during phagocytosis’ focus on the 2 phases of pseudopod extension that included actin polymerization pushing the membrane forward and increased membrane tension using high-resolution microscopy of macrophages attempting to internalize an IgG-opsonized glass surface. A 50% increase in tether force was observed in phagocytic cells, compared to the resting cells membrane tension. Additionally, inward bead movement (engulfment) and ingestion is most probably due to contraction and exocytosis activation. This confirms that membrane tension is an exocytosis activator and that exocytosis is required for phagocytosis to complete.

Reference <pubmed>23821745</pubmed>| Pubmed

Copyright @2013 Masters et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation: ‘Plasma membrane tension orchestrates membrane trafficking, cytoskeletal remodeling, and biochemical signaling during phagocytosis' Thomas A. Masters, Bruno Pontes, Virgile Viasnoffa, You Li, and Nils . Gauthier, (2013) Proc Natl Acad Sci U S A. 2013 Jul 16;110(29):11875-80. doi: 10.1073/pnas.1301766110. Epub 2013 Jul 2.

trans-endocytosis

Images

--Z3375490 (talk) 15:13, 3 April 2014 (EST)

[[2]]

[[File:Pnas.1301766110fig01.jpg]

--Z3420257 (talk) 22:24, 1 April 2014 (EST)

Insulin-DependentEndo.png

Localization of insulin receptor and caveolin-1 in endosomes by immuno-gold electron microscopy. Isolated adipocytes were incubated with insulin at 100 nM for 10 min. Cells were then homogenized and the endosomal fraction isolated. Endosome vesicles were attached to grids, immunogold-labeled against caveolin-1 (6 nm gold particles) and the insulin receptor (15 nm gold particles), lyophilized and sputtered with a 2-nm tungsten film before examination by transmission electron microscopy. C and D are blow-ups from B; arrowheads indicate patches of caveolin-1 labeling; arrows indicate insulin receptor labeling. One experiment of three with similar results is illustrated. doi:10.1371/journal.pone.0005985.g004

Reference

<pubmed>19543529</pubmed> | PLOS One

Copyright

© 2009 Fagerholm et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Note - This image was originally uploaded as part of a student project and may contain inaccuracies in either description or acknowledgements. Please contact the site coordinator if the uploaded content does not meet the original copyright permission or requirements, for immediate removal.


--Z3373930 (talk) 11:37, 3 April 2014 (EST)

px300

Image showing effects of dynamin on FGF1 internalisation.

Figure 3: The effect of dynamin 1, dynamin 1 K44A, dynamin 2 or dynamin 2 K44A expression on FGF1 internalization. U2OS cells stably transfected with FGFR1 (A) or FGFR3 (B) were transfected with HA-tagged dynamin constructs as indicated and incubated with Cy3-FGF1 and 50 U/ml heparin at 37°C for 20 min. The cells were then fixed and stained with anti-HA antibody. The cells were examined with confocal microscopy. Bar, 5 µm. doi:10.1371/journal.pone.0021708.g003

Reference

<pubmed>21779335</pubmed>

Copyright

© 2011 Haugsten et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


--Z3399239 (talk) 14:22, 3 April 2014 (EST)

Uptake of MIF via CPZ sensitive endocytosis.png

Image of Uptake of MIF via CPZ sensitive endocytosis

Reference

<pubmed>PMC3026819</pubmed>

Copyright

© 2011 Xie et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.