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

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<pubmed>20862315</pubmed> [http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1001110 | PLoS One]
 
<pubmed>20862315</pubmed> [http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1001110 | 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 establish 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.  
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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===
 
===Human Cytomegalovirus Entry into Dendritic Cells Occurs via a Macropinocytosis-Like Pathway in a pH-Independent and Cholesterol-Dependent Manner===

Revision as of 13:55, 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.


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 doral 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.