From CellBiology

Gabriel Nedel Duarte

Lab atendance

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PMID 25513760


Individual Assessments

Lab 1


Bacteria associated with archaea Copyright Baum and Baum; licensee BioMed Central Ltd. 2014

Lab 2


Example of epibiotic bacteria associated with archaeal cells. Image of two Candidatus Giganthauma karukerense cells surrounded by ectosymbiotic γ-proteobacteria [1]


  1. <pubmed>25350791</pubmed>


Motility of fungal nuclear pores. Clustering of nuclear pores occurs in the absence of microtubules. [1]


  1. <pubmed>3413351</pubmed>

The Article uses super-resolution microscopy in order to try to get images of the nuclear pore complex (NPC) so as to determine it's structure. This is a tough work, considering the fact that you got a huge amount of protein assemblies and it's so far unknown wich spot each protein occupies in these complexes. However, researches thought that just the SRM itself wouldn't be able to set their goal, as in situ biological structures present a maximum resolution of 6-8nm, but then they decided to gather individual complexes' images of each particle, finding their proper positions via antibody labelling and other techniques, and finally putting them together in order to get the structural organization. <pubmed>23845946</pubmed>

Lab 3


Search term: ["Fibronectin" ]

biomed central


1. Therapeutic vaccination against fibronectin ED-A attenuates progression of metastatic breast cancer. A substitute to the nowadays common cancer therapy (monoclonal antibody) consists on the therapeutic vaccination targeting self-molecules. Fibronectin, a compound from the Extra Cellular Matrix has got two alternatively spliced extra domains (ED-A and ED-B) which are expressed during embryogenic angiogenesis, however it practically disappears in normal adults. Nonetheless, the ED-A and ED-B are detectable in tumors’ angiogenesis and also in matrix remodelling. The study showed that mice who were injected with anti-ED-A/B tend to have less metastasis, as well as immunization against ED-B diminished angiogenesis and tumor growth. ED-A is known to be expressed at hight levels in human breast carcinomas (researches developed a transgenic model of human ductal carcinoma in the mice in order to have a trustworthy comparsion) and general metastasis, whereas ED-B shows very low leves in this types of tumors. The immunization of the mice with anti-ED-A reduced tumor burden and the metastasis diminished/suppressed. [1]


  1. <pubmed>25360764</pubmed>

2.Human fibroblasts with mutations in COL5A1 and COL3A1 genes do not organize collagens and fibronectin in the extracellular matrix, down-regulate alpha2beta1 integrin, and recruit alphavbeta3 Instead of alpha5beta1 integrin. Patients with Ehlers-Danlos Syndrome types I and IV who got mutations in COL5A1 and COL3A1 present diminished Fibronectin(FN) as well as its fibrillary network. Research showed that by providing pure fibronectin to EDS patients, there was a proper binding and gathering between FN and integrin αvβ3, wich is expressed in every EDS cell instead of the normal α5β1 integrin. [1]


  1. <pubmed>14970208</pubmed>

3.Fibronectin is overproduced by keloid fibroblasts during abnormal wound healing. Study compared the levels of fibronectin in normal tissue against wounds that developed keloid, a process which consists on an over-production of collagen and other extra cellular matrix components. The keloid tissue presented a huge production of both intra and extracellular fibronectin (due to its mRNA increment), that had no abnormalities in the structure, process and degradation. The fibronectin receptors also raised in the abnormal tissue. When administrated glucocorticoids, fibronectin production was stimulated in both normal and keloid fibroblasts; however, in the last one we had less stimulus. [1]


  1. <pubmed>2524650</pubmed>

4.Mutations in FN1 cause glomerulopathy with fibronectin deposits. Glomerulopathy with Fibronectin (GFND) deposits is a dominant inherited disease that affects the kidney, causing some peculiar symptoms as loss of protein and presentation of red blood cells in the urine, hypertension and is most of all due to deposits of FN in the glomerulus. Researchers had a theory that the etiologic cause of GFND might be due to mutations in the FN1, an encoder of FN. The study found a connection between FN1 and GFND when analysing a Italian pedigree. By sequencing the FN1 from other pedigrees, three missenses mutations where found and seemed to alter two domains of FN1, which are mainly related to the binding of FN and the target cells, as well as in the fibrillogenesis. About 40% of the GFND in the study where due to dominant mutations in FN1, and this was described for the very first time. [1]


  1. <pubmed>18268355</pubmed>


Fibronectin accumulation in normal and keloid fibroblasts. Figure A: Cell stained for extracelular FN. B: Both intra and extracelular FN.



  1. <pubmed>2524650</pubmed>

Lab 5


Lab 9

ATCC: Murine pneumonia virus

keratinocyte; human papillomavirus 16 (HPV-16) E6/E7 transformed

ECACC: AB1 Mouse malignant mesothelioma

Human T-cell leukemia [1]

culture medium: RPMI 1640 + 2mM Glutamine + 10% Foetal Bovine Serum (FBS).

minimal essential meidum:

Penicillin- streptomycin spectrum: It accords broad spectrum bacteriocidal activity against both gram positive and gram negative bacteria

Group 1 Peer Review

Group 1, your project seems to be very organized and well explained, regarding each subtopic you guys presented. The fact that you chose four of the SLRP came to vary even more the information given, making the work richer. I see in Lumican there are some missing info but surely you will come up with something; the diseases section is very complete as you contemplated a vast number of topics. The images were well selected as well as the charts. I think the layout of decoryn and byglycan and fibromodulin and lumican can be improved, maybe by heading hyphens or highlighting the function, structure etc in order to look more organized and have a better visual appearance.

Group 2 Peer Review

Group 2, the keypoints seem to be well described, as well as the content, headings and subheadings. The association between integrins and other ECM compounds was very creative and gave extra good information. When it comes to the disease topic, I think you guys explored it well, giving good explanation on a more specific way, interrelating cancer subjects with cell biology ones accurately. The images, graphic and the video feet just perfect, showing on a simple but easy to understand way. However, I think the general structure lacks a bit more of fluidity; you could organize some topics into dot points, for example, and regarding the disease topic, I think some info can be more summarized as it is a very long topic.

Group 3 Peer Review

Group 3, overall you guys have made a pretty good and solid work. The structure, headings and subheadings are well explained, I just think there could be somethings about the history of some of the elastic fibres, as well as current research and treatment can be contemplated. The drawing was so far the best I have seen among the groups and the other images are very elucidative, I just think you could add something extra to the clinical significance to give a break on the reading as there is a lot of information. Furthermore, I think you could have some more extra references; that would enrich your work even more. Apart from that the rest is looking really good. Nice job!

Group 5 Peer Review

Group 5, overall the presentation of your project seems quite messy and unorganized. Some topics are repeated along the presentation, like the function and defects/abnormalities sections and that could be cut off. The referencing below each heading breaks completely the fluidity of the project, I am sure you guys are going to fix it. The structure heading is all right, well explained and with some good pictures. However, the function topic is too long and incomplete, maybe you should just focus on the 3-5 main laminins. Abnormalities section looks pretty good, with punctual and clear information. Current research is too long, almost a third of the overall, maybe some information could be better summarised. If you focus on clarity and on simplicity this project will become a very good one.

Group 6 Peer Review

Group 6, overall the project has got missing topics and lack some organization but I’m sure you will come up with something to fix it. Abnormalities section is quite confusing and unorganized, specially the Kniest Dysplasia, because it seems the information given was just dropped randomly. I think you guys could explore more the diseases by giving some brief information on the clinical manifestations and the main reason collagen type II is related to it. The antibodies subheading could be less specific, maybe just mention the ones you judge to be more clinical or scientifically important. Current understanding and research areas are quite well and has got good explanation, good job on that one!

Group 7 Peer Review

Group 7, despite of some lacking information which I believe you will be posting on the following days, your project seems very well organized and explained, contemplating the general content with interesting headings, subheadings and images. The function topic is a bit unorganized; maybe you could first mention the function itself and then talk about the heterogeneity. The abnormalities/diseases topic is well elucidated, as well as the formation, plasticity and regeneration. The functional layers could be further contemplated with some extra information and so does the structural components.