Gpruett2 (talk) 07:05, 13 February 2013 (UTC)

Hakkinen2013

"I'm editing Wikipedia as part of this assignment and here's a link to my sandbox."

Welcome

I hope you get in and off the wait list. =) I'm your online ambassador. Since you're interested in medical stuff, check out the discussion at

Also those quotes on your user page are unnecessary. ;-) Biosthmors (talk) 20:01, 23 January 2013 (UTC)

Nice to meet you Biosthmors!Thanks for the link! I wish I had more time, but with work at the Wash U. and this being my first semester back in classes in two years I have had sorta a slow start to getting back in the swing of things.

I will say that I am looking forward to this Wikipedia project for class and always have been curious about the many ways to utilize wikipedia. To say the least I am in a state of awe at this moment with it.

With all the time constraints in my current life I am sure that I will be asking you many questions and for feedback about my noobish early edits/additions.

I try to make very dry jokes at every opportunity hence the strangeness that is my current self page. "Don't be surprised if you see more."

-Hakkinen2013 11:30 on 12313

Nice to meet you too! You're welcome. I'm glad you're looking forward to editing! Please feel free to ask me for help anytime at my talk page. The help desk and Teahouse are also available for you. Just type "WP:" in front of help desk or teahouse to get to either of those two places in the Wikipedia search bar. Sounds good! =) Ah, and also see

WP:CHEAT for how to sign talk pages. There's a way to do it with one click too, right above the edit summary box when you click edit. Best! Biosthmors (talk

) 21:53, 28 January 2013 (UTC)

talk pages and Wikipedia pages that have open discussion, you should sign your posts by typing four tildes ( ~~~~ ) at the end of your comment. You could also click on the signature button or located above the edit window. This will automatically insert a signature with your username or IP address and the time you posted the comment. This information is useful because other editors will be able to tell who said what, and when they said it. Thank you. --SineBot (talk

Jnims (talk) 21:50, 18 February 2013 (UTC)

Assignment 3

Everything looks good so far! — Preceding unsigned comment added by Flemingrjf (talk • contribs) 05:32, 19 February 2013 (UTC)

Assignment 3 copy editing

I noticed in your citing that you have the same reference cited multiple times as many different numbers. In order to have one reference per number, use the following format: < ref name=first author's last name> citation <ref/ > and then < ref name=author's last name/ > to cite again. If you want an example of this, I have it in my article edit in my sandbox. Gpruett2 (talk) 04:10, 21 February 2013 (UTC)

Assignment 5 Peer Review

This first part will be in regards to the entire article as a whole, and then what you have edited. I didn't want to change anything without your thinking it over first, so most of the major things, I will tell you about. The minor ones I went to go in and fix.

• The first thing I noticed was the structure of the article didn't seem to be the best. There is a template about cell signaling pathways that begins with the history/discovery, then the mechanism, then the role, then the human diseases, associated with that structure or pathway, and then the research that is currently being performed on the structure and mechanism. Hopefully this will be a good place to begin. It worked very well for my topic.

• Also that list of human adhesion proteins seems like it is sort of in the way and doesn't provide much to the overall article. Maybe putting it towards the end of the article would be good, as a source where people can go and check on one of the many adhesion proteins.

• There were many places that I felt citations should be made. I was originally going to go through sentence by sentence where I felt there should be citations, but I feel like you know where they should be made. The entire section regarding cleavage had only a couple citations that I felt were not necessary. I completely redid that paragraph as will become apparent later.

• I also moved some citations from the beginning of paragraphs to the end of them, as the one citation was referring to the entire paragraph and not just the first sentence.

• For the first paragraph under signaling, you indicate a technique used for the identification of molecules interacting with the GPCR. However, I feel like citing this technique with a paper that used the technique would be beneficial for people to see how it was done.

• I added citations towards the ends of the paragraphs about the two adhesion proteins listed in the third and fourth paragraphs. I also have an idea that would dramatically change the structure that I will talk about a little bit further on.

• The cleavage section needed a whole overhaul of the language that was used. I felt it was much to confusing and complex for many reasons. I have tried to make it so that a causal viewer can come upon the page and read it with good understanding. If a more advanced person wants knowledge, I feel that that is when they should go to the citations. Also, there were only three citations in this entire section and they all referred to other organisms where the GAIN domain is found. I thought this sentence to be pretty useless and have taken it out, among many other words that I felt were unnecessary. If you don't like the change, feel free and put it back the way it was. I feel that this is more of the style that Wikipedia is going after, however. I didn't want to go in and change everything about the article, but I wanted to provide this as an example for how it should be done I feel. The page is yours, however, so feel free to make the changes you feel should be made. I am just providing that as an example.

• The section on the immune system I found to be very hard to read. As someone with some background knowledge regarding biology at this level, I still found it very difficult to read through.

• The sentence regarding the BAI1 adhesion protein, I redid as well. I thought that by stating what the protein was thought to be involved in and then stating what it actually is involved in was too similar to the review article this came from. It also, at least for me, adds nothing to my knowledge and current understanding about the protein if it is listed about what the protein was thought to have been involved in.

• I liked the way the GPCR adhesion protein GPR126 was described in the Neuronal Development section. I liked that it had multiple citations, and the way the information on this page was written was not anywhere similar to the way that it was presented in the articles that cited it. I thought that was very well done.

• I didn't like the way that GPR56 was addressed in the entire article. Little pieces of it are found everywhere. A paragraph is devoted to it in the ligand section. There is a sentence about it in the immune system section, a sentence about it in the bone marrow section, and a sentence about it in the bilateral frontoparietal polymicrogyria section. This brings me to a main point that I had regarding the article as a whole. I feel that a much better structure for this article were to describe each GPCR adhesion protein as if it were its own perhaps mini article, where the ligands, signaling, functional roles, and roles in disease were all put into one section that was all under the heading of the GPR56. Perhaps a better method would be to even put most of this information in the GPR56 page of wikipedia. I also noticed with the GPR12 protein, there was more information on the GPCR adhesion protein in this article than there was on the actual GPR12 article itself. It might be hard to figure out where the information should go, especially if you are trying to fix the main article, regarding ahesion GPCRs. I went searching on Pubmed for general review articles about adhesion GPCRs and found several that seemed to be very good places to begin, as a sort of overview of the GPCR adhesion proteins in general. It seemed like many of the articles that you have cited are primary articles, that could be very dense and hard to get through, while coming to a conclusion that yields the same knowledge that one sentence of a review article could provide. Those primary articles also seem to focus in on one mechanism or structure of one GPCR adhesion protein without addressing what you want to be addressing, which is the overall view of GPCR adhesion proteins.

• This leads me to another very important point, which is that the way you cited the articles, one on Wikipedia is not simply able to follow the link to a website such as
  Pubmed. I have included where you can use citations for the Pubmed journal articles Wikipedia template filling tool
  . I will do a couple for you. When doing this, you need to make sure you press the "Add ref tag" button below. I think it is very important to make them so you are able to follow the link to the article online. I feel that this is very important for someone who is doing some research of their own and have gone to Wikipedia as a starting place. In the past, I have gone to a Wikipedia page to mainly look for articles that were cited at the bottom of the page and not pay heed to the information that was presented at the top.

Flemingrjf (talk) 07:56, 25 March 2013 (UTC)

Help us improve the Wikipedia Education Program

Hi Hakkinen2013! As a student editor on Wikipedia, you have a lot of valuable experience about what it's like to edit as a part of a classroom assignment. In order to help other students like you enjoy editing while contributing positively to Wikipedia, it's extremely helpful to hear from real student editors about their challenges, successes, and support needs. Please take a few minutes to answer these questions by clicking below. (Note that the responses are posted to a public wiki page.) Thanks!

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Hello

Hey there how's your assignment going? I was looking at that and I thought "have been shown to" could be removed (copy-edited out). Also, if this is a tentative report ("possibly interact") then is it worth mentioning? Might we be better off to wait on a secondary source (if it is based on one primary report) lest it is contradicted soon? I'm not knowledgeable on the literature. Just some thoughts! I hope you're doing well. Best. Biosthmors (talk) 12:53, 21 April 2013 (UTC)

My apologies

I see that you put

cAMP is an amazing second messenger necessary for myelination in Mouse Schwann cells [1]

Assignment 2

Proteasome

"The proteasome most exclusively used in mammals is the cytosolic 26S proteasome, which is about 2000 kilodaltons (kDa) in molecular mass containing one 20S protein subunit and two 19S regulatory cap subunits." I would like to edit this to be...

The proteasome most exclusively used in mammals and found "exclusively in Eukaryotes" ^[2] is the cytosolic 26S proteasome, which is about 2000 kilodaltons (kDa) in molecular mass containing one 20S protein subunit and two 19S regulatory cap subunits.

The talk page as had a section added about the S26 proteasome Talk:Proteasome

Links to my three page edits and comments

Adhesion-GPCRs , Talk:ErbB , Talk:EGR1

here is a link to my edit for Adhesion-GPCRs [39] and ErbB 2 and finally EGR1 3

Link to my added info for

Wikipedia talk:WikiProject Cell Signaling

Link to my added info for User talk:Biolprof

Assignment 3

I will be mock adding to two headings in the

Ligand A majority of the Adhesion GPCRs are orphan receptors and work is currently underway to de-orphanize as many of these receptors as possible.^[3] Adhesion GPCRs get their name from their N-terminal domains that have adhesion-like domains, such as EGF.^[3] While ligands for many receptors are still not known, researchers are utilizing drug libraries to investigate compounds that can activate GPCRs and using these data for future ligand research.

Signaling Adhesion GPCRs follow standard

Gα12/13

. As of today, many of the 800 Adhesion GPCRs are still orphan receptors and their signalling pathways are also not identified. Research groups are working to elucidate the downstream signaling molecules utilizing several methods, including chemical screens and analysis of second messenger levels in over-expressed cells. Adding drugs in vitro, while the cells are over-expressing an Adhesion GPCR has allowed the identification of which molecules are activating the GPCR and the second messenger it is utilizing.

I am trying to figure out a way to cite a source only once and then reuse the citation number over instead of it becoming a new citation each time.

I believe you just reuse the ref tags from the previous citation (so that they're exactly the same) and it will show up under the same number. Maybe also ask Grace, as she is our group's Wikipedia point person.

got it thanks!

All comment changes considered and changed. Thanks for all the suggestions.

Assignment 4

Evolution of Adhesion GPCRs: Adhesion GPCRs are found in

Role in disease: BFPP Mutations in GPR56 result in bilateral frontoparietal polymicrogyria in humans, characterized by abnormal neuronal migration and surface ectopias.^[7]

Signaling Adhesion GPCRs follow standard

GPR56 knockout mice have a decreased number of hematopoietic stem cell in the bone marrow, while higher levels were found in the spleen and peripheral blood.^[10] This suggest that GPR56 plays a role in interactions between bone marrow and hematapoietic stem cells.

Neuronal development

Cross Talk

GPCRs downstream signals have been shown to interact with integrin signals, such a FAK. ^[13] (in GPCR page)

Diffs

GPCRs: cross talk [40]

Adhesion-GPCRs: [41]

future papers

• A novel evolutionarily conserved domain of cell-adhesion GPCRs mediates autoproteolysis

• Integrin and GPCR Crosstalk in the Regulation of ASM Contraction Signaling in Asthma

Assignment 7

VlgR1:

The adhesion GPCR Very Large GPCR receptor 1 (Vlg1R1) is the largest GPCR known, with a size of 6300 amino acids and consisting of 90 exons.^[14] There are 8 splice variants of VlgR1, named VlgR1a-1e and Mass1.1-1.3. The N-terminus consists of 5800 amino acids containing 35 Calx-beta domains, one pentraxin domain, and one epilepsy associated repeat. Mutations of VlgR1 have been shown to result in Usher's syndrome. Knockouts of Vlgr1 in mice have been shown to phenocopy Usher's syndrome and lead to audigoenic seizures.

The

The adhesion GPCR BaI3 is an orphan receptor that has a long N-terminus consisting of one cub domain, five BaI Thrombospondin type 1 repeats, and one hormone binding domain.[16] BaI3 is expressed in neural tissues of the central nervous system. BaI3 has been shown to have a high affinity for C1q proteins. C1q added to hippocampal neurons expressing BaI3 resulted in a decrease in the number of synapses.

CD97:

CD97 is an adhesion GPCR that is normally found on tissue of hematapoetic origin and in smooth muscle.^[17] It signals through Gα12/13 and activates RHO. It has been found to be upregulated in Cancers, including prostate, breast, and thyroid. In prostate cancer. it has been shown that CD97 is hetoerodimerizing with another GPCR, LPAR. The interaction is believed to further enhance the RHO signaling between both receptors.^[18]

GPR56 expanded:

GPR56 has been shown to be cleaved at the

EGF-like module-containing mucin-like hormone receptor-like 2 (EMR2) is an adhesion GPCR that undergoes GPS autoproteolysis before being trafficked to the plasma membrane.[20] Mutations in the GPS have shown that EMR2 does not need to undergo autoproteolysis to be trafficked, but loses function. EMR2 has been shown to be necessary for in vitro cell migration.

Upon cleavage the N-terminus has been shown to associate with the 7TM, but to also dissociate, giving two possible functions. When the N-terminus dissociates it can be found in lipid rafts. Additionally, the cleaved EMR2 protein 7TM has been found to associate with EMR4 N-terminus.

GPR64:

The adhesion GPCR, GPR64, is an orphan receptor characterized by a long N-terminus with that has been suggested to be highly glycosylated.^[21] GPR64's N-terminus has been reported to be cleaved at the GPS domain to allow for trafficking to the plasma membrane. After cleavage the N-terminus is believed to remain non-covalently associated with the 7TM. Male mice lacking GPR64 are infertile.

GPR64 expression has been mostly reported in the male reproductive organs, but more recently has been shown to be expressed in the central nervous system.^[22]

Reorganization of the Adhesion GPCRs:

There are 33 human adhesion GPCRs that can be broken down in the 8 groups and 2 independent receptors. Group I consists of

    I will consider changing the format with headings, but most likely not until the final set of revisions.

     Moved.

     I have the mind set that one citation for relevant chunk of information should be fine, but I will add more where there are strong assertions.   I did not write the cleavage section, but thank you for editing it.

     sure that works just as well.

      I will see what I can find.

     Nice and thank you.

     That section was again not written by me but I will follow your lead and put some more focus on adding clarity to it.

    Again not written by me, but I will work on that one too.  

    Why thank you.

    I will mull this over for a few days and then maybe make the moves as you suggest.

    I need to add more to it.

as of 4/16/2013 Adhesion GPCR

GPR64 diffs

EMR2 diffs

CD97 diffs

BAI3 diffs

VLGR1(GPR98) diffs

Assignment 8

part 1 peer review

These are responses to comments from Biosthmors as I did not find Grace's suggestions.

1. I will see what I can do with the rewording of the intro paragraph: In the lead paragraph, I am deleting the first paragraph because it is repeated in a later section. This should help shorten the lead. Other changes may follow. I feel the lead offers a good "abstract" style for the article and although it may be long is informative for those that would like to skim and get a general idea of what Adhesion GPCRs are.

2. I added adhesion g protein coupled receptor to the beginning.

3. The not so recent work that recently says "recently" is not mine, but that recent work will soon become recently changed. The current work of mine that currently says currently in two places is currently about to be changed concurrently of one another.

4. Super- means very large combined with family meaning all those persons considered as descendants of a common progenitor. Redirecting to protein family should be enough.

5. Not my work, but I will correct it. I think metazoans is fine as people should learn what it means... I will link it as well.

6.I would agree a table may be better, but I think for now it is fine.

7. I left it in for a quick reference at the bottom, but will delete it.

8. yes? The proposed part was removed seemed a little strange.

10. Thank you!

11. Possibly in future revisions

12. I think Adhesion-GPCR is good for now as a tittle, but that is something that I think people should know what GPCR stands for and can easily find out.

Here are the Difs

part two peer review of other articles

All suggestions are made on the peer review area of each article.

-Matt's plant article is very well done and I do like his use of bullet points. I have no comments as of now to add to the plant article section.

-Caitlin's SR protein article: -linked metazoans. -I think the last line of the lead could be put else where.

-Max's small vesicles is pretty good covers a broad range of topics and gives insights into not just signaling and mechanisms of release, but into disease implications as well. No comments or changes as of yet.

-Julia's GST article: -"GSTs can constitute up to 10% of cytosolic protein in some mammalian organs" would it be possible to say what organs?

-Grace's WNT is good.

-Bobby's mTor: -There are some differences with the bold font for titles of sections.

References

Arthur-Farraj, P., Wanek, K., Hantke, J., Davis, C. M., Jayakar, A., Parkinson, D. B., Mirsky, R. and Jessen, K. R. (2011), Mouse schwann cells need both NRG1 and cyclic AMP to myelinate. Glia, 59: 720–733. doi: 10.1002/glia.21144

Jnims

I am editing Wikipedia as part of this assignment for my first semester of graduate school at SLU. Here is a link to my sandbox.

Assignment 2

[42] [43] [44] [45]

Assignment 3

I have selected Glutathione S-transferase as my main project article.

Assignment 4

[46] [47] [48] [49] [50] [51]

Assignment 6

I realize I haven't added 8 paragraphs of content, but I have moved things around, responded to and complied with suggestions, created new sections, worked on cleaning up the article, etc., in addition to adding three or so new paragraphs. I hope it will suffice, for now. Jnims (talk) 04:55, 19 April 2013 (UTC)

Responses to Ian's suggestions: [52]

Responses to Grace's suggestions: [53]

Article changes: [54] [55] [56] [57] [58] [59] [60] [61] [62]

Welcome

Nice work uploading a picture already! Welcome. Biosthmors (talk) 20:06, 23 January 2013 (UTC)

And if you want to "officially" display the template that says "This user is a member of WikiProject Molecular and Cellular Biology" then you should put it on your user page, User:Jnims. Best! Biosthmors (talk) 20:07, 23 January 2013 (UTC)

Article topic for Biol 512

Taking a quick look at the links you posted on my talk page, it looks like you've found some good resources and I agree with your assessment about editing the

The information looks good from a good search and search through your articles in the posted references. I would like to have the references added to your current ref section and them inserted next to the relevant sentences. Hakkinen2013 (talk) 04:28, 19 February 2013 (UTC)

Assignment 3

I agree with Ian. I have learned that keeping track of the citations right off the bat has always helped organize things much better. It saves much wasted time trying to go back and figure out where each source came from and then just giving up trying to figure it out. This may seem like common sense, but I still have yet to get this idea fully incorporated into my own research as of yet. Flemingrjf (talk) 05:36, 19 February 2013 (UTC)

Assignment 3 feedback

Thanks for the suggestions, Ian and Bobby. Actually, all the information I got came from that one citation, but I plan to expand it in the future, of course.

Jnims (talk) 19:35, 19 February 2013 (UTC)

Assignment 3

Your formatting looks to be in good shape. Keep up the good work. Gpruett2 (talk) 04:24, 21 February 2013 (UTC)

Reply

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Biosthmors (talk) 05:17, 19 March 2013 (UTC)

Assignment 5

Ian's Review of Glutathione S-transferase

Julia's responses below each of Ian's points, below. Jnims (talk) 21:09, 17 April 2013 (UTC)

Your work:

(structure)

• Add a Citation end note in the first paragraph. I think it would be reference 7 again there. From the 2011 Glutathione transferases: a structural perspective paper
  • Right you are. Done.

• the UniProtKB/Swiss-Prot database can be linked as
  uniprot
  • Done.

• I am a little bit confused by the maxed all species column. Does it mean that that is highest number that has been found out of all species? (the chart is good otherwise)
  • That's a great question! I have absolutely no idea, and am wholly unfamiliar with protein databases. I will try to contact the user who made the chart originally, in the hope of gaining insight.

• Good information. The second paragraph may be a good place to add more for your next revision, possibly expanding and adding more details about the information that you already have.
  • Thanks; I will focus on this area for Assignment 6.

(role in cell signaling)

• Paragraph 1 is a good intro and set up for what comes.
  • Thank you kindly.

• paragraph 2 needs a citation where you say "in fact"
  • Done.

• I think each example you give about the different classes of GST provides good details and that is the best way to do it.
  • Excellent, thanks.

(implications in cancer)

• Nice picture for the possible ways that GST can play a role in cancer.
  • Thanks; I thought so, too.

The Previous Material:

• I find the introduction to be a bit wordy and confusing. It took me several reads to get a gist of what is trying to be said. A possible place for revisions in the future.
  • I agree, and will work on improving it for Assignment 6.

• The Gst and Biotransformation heading could be just biotransformation.
  • Good point. Done.

• There is a logical flow to the article and it definitely is a good start for this addition.
  • Thanks!

— Preceding unsigned comment added by Hakkinen2013 (talk • contribs) 04:39, 26 March 2013 (UTC)

Help us improve the Wikipedia Education Program

Hi Jnims! As a student editor on Wikipedia, you have a lot of valuable experience about what it's like to edit as a part of a classroom assignment. In order to help other students like you enjoy editing while contributing positively to Wikipedia, it's extremely helpful to hear from real student editors about their challenges, successes, and support needs. Please take a few minutes to answer these questions by clicking below. (Note that the responses are posted to a public wiki page.) Thanks!

Delivered on behalf of User:Sage Ross (WMF), 17:14, 10 April 2013 (UTC)

Assignment 5 feedback from Gpruett2

Grace was kind enough to provide suggestions for me, as well, so I've included them below, followed by my responses. Jnims (talk) 00:49, 18 April 2013 (UTC)

• The first big thing that I note is that several paragraphs that you did not edit (the ones under “GSTs and biotransformation” and “GST-tags and the GST pull-down assay”) and one that you did (first paragraph under “Structure”) have no citations. These paragraphs list specific information; thus, it is vital that they be cited.
  • I will try to find citations for the content I did not add. I've added a citation to the Structure section.

• Another issue that I noted is that while one section is titled “Structure”, I feel like it is mostly discussing how GSTs are divided into different classifications. I would suggest either separating the information about structure and classification into two different sections or re-labeling this section.
  • Good point. From your suggestion, I have decided to separate the information into two sections: Structure and Classification.

• Furthermore, you should consider rewording the first paragraph under “Structure”. Specifically, make sure that it is obvious that GST proteins are classified as belong to one of the three different families (cytosolic, mitochondrial, or MAPEG). I say this because when I first read this paragraph, I wasn’t sure of how the sentences starting with “Cytosolic GSTs”, “Mitochondrial GSTs”, and “The MAPEG superfamily” related to one another.
  • I have attempted to clarify the wording.

• Also, while the writing is very sound and the information in the different sections are relevant to one another, I feel like a lot of the paragraphs under your sections seem rather disjointed. They do not transition well between each other. For example, under “Role in Cell Signaling”, you go from talking about the effects of GST on MAPK signaling to talking about the location of GSTπ. For me as a reader, I find this distracting and confusing. To remedy this, perhaps start the GSTπ paragraph with an introduction sentence that mentions it is related to cell signaling. Overall, with all of the paragraphs that are together under a section, try to make them flow together.
  • I will work on knitting the sections together more effectively, although I believe the GSTP paragraph is fine as it stands, as the second sentence relates it to cell signaling. I tried in the past to make it more obvious, but could not find a good way to include all the necessary information about the meaning of the name "GSTP1-1" without putting off the cell signaling tie-in until the second sentence.

• Generally, I also suggest that you might want to reconsider the overall structure and organization of your article. The
  WikiProject Molecular and Cellular Biology Style Guide
  has a good suggestion for the different sections that should be included in a protein article.
  • I am currently working on a Function section, and would also like to add a section about the history/discovery of the protein superfamilies, if possible. Additionally, I would like to include a Clinical significance section, as you suggest below. While a Gene section is in theory appealing, the huge array of isozymes and superfamilies and classes of GSTs may make such a section of dubious value.

• Specifically, you should probably move the “Role in cell signaling” and “Implications in cancer development” sections out from under “Structure”. They do not seem to be specifically related to structure and/or they do not really discuss structure; thus, they should not be listed under structure.
  • I hadn't even noticed that. Thanks! It is fixed.

• I also moved one of your citations. I place citation [8] next to citation [9] at the end of the sentence because that is where I believe Wikipedia likes to have citations.
  • Much obliged.

• I also have some suggestions for sections that you might want to include in your article. One such section would be “Clinical significance” or “Implications in disease”. This would be a good section to not only discuss GST involvement in cancer, but also other conditions. For instance, citation [4] lists several other conditions (such as Parkinson’s, Alzheimer’s, and cardiovascular disease) that are associated with malfunctioning GST. Another useful section would be a “History” or “Discovery” section. While Wikipedia asks that you not specifically list who conducted each study in GST, it does say that you can mention those who made key discoveries. Also, this section could discuss what experiment was used to first discover GST.
  • I would like to create both of these sections (see above). Thank you for the suggestions!

This is the user sandbox of Biosthmors. A user sandbox is a subpage of the user's user page. It serves as a testing spot and page development space for the user and is not an encyclopedia article. Create or edit your own sandbox here. Other sandboxes: Main sandbox | Template sandbox Finished writing a draft article? Are you ready to request review of it by an experienced editor for possible inclusion in Wikipedia? Submit your draft for review!

This is my test sentence. Here^[1] is an article about signal transduction.

Useful links

Course page

Avoiding plagiarism

Reference template tool

Instructions for reference template tool

Citation tools

National varieties of English

Project article: Glutathione S-transferase

Assignment 3

Glutathione S-transferase structure

Protein sequence and structure are important classification methods for GSTs: while classes from the cytosolic superfamily of GSTs possess more than 40% sequence homology, those from other classes may have less than 25%. Cytosolic GSTs are divided into 13 classes based upon their structure: alpha, beta, delta, epsilon, zeta, theta, mu, nu, pi, sigma, tau, phi, and omega. Mitochondrial GSTs are in class kappa. The MAPEG superfamily of microsomal GSTs consists of subgroups designated I-IV, between which amino acid sequences share less than 20% identity.

The glutathione binding site, or "G-site," is located in the thioredoxin-like domain of both cytosolic and mitochondrial GSTs. The region containing the greatest amount of variability between the assorted classes is that of helix α2, where one of three different amino acid residues interacts with the glycine residue of glutathione. Two subgroups of cytosolic GSTs have been characterized based upon their interaction with glutathione: the Y-GST group, which uses a tyrosine residue to activate glutathione, and the S/C-GST, which instead use serine or cysteine residues.^[2]

Bibliography of relevant research

Glutathione transferases: a structural perspective

Glutathione transferases as mediators of signaling pathways involved in cell proliferation and cell death

Assignment 4

Ideas (TEMPORARY):

• Infobox detailing orthologous structure in human genome as per
  GNF protein box
• Gene information

Structure

Protein sequence and structure are important classification methods for GSTs: while classes from the cytosolic superfamily of GSTs possess more than 40% sequence homology, those from other classes may have less than 25%. Cytosolic GSTs are divided into 13 classes based upon their structure: alpha, beta, delta, epsilon, zeta, theta, mu, nu, pi, sigma, tau, phi, and omega. Mitochondrial GSTs are in class kappa. The MAPEG superfamily of microsomal GSTs consists of subgroups designated I-IV, between which amino acid sequences share less than 20% identity.

The glutathione binding site, or "G-site," is located in the thioredoxin-like domain of both cytosolic and mitochondrial GSTs. The region containing the greatest amount of variability between the assorted classes is that of helix α2, where one of three different amino acid residues interacts with the glycine residue of glutathione. Two subgroups of cytosolic GSTs have been characterized based upon their interaction with glutathione: the Y-GST group, which uses a tyrosine residue to activate glutathione, and the S/C-GST, which instead use serine or cysteine residues.^[2]

The

Although best known for their ability to conjugate GSH and thereby detoxify cellular environments, GSTs are also capable of binding nonsubstrate ligands, with important cell signaling implications. Several GST isozymes from various classes have been shown to inhibit the function of a kinase involved in the MAPK pathway that regulates cell proliferation and death, preventing the kinase from carrying out its role in facilitating the signaling cascade.^[3]

The cytosolic π-class GST composed of subunit 1 homodimers (GSTP1-1), a well-characterized isozyme of the mammalian GST family, is expressed primarily in heart, lung, and brain tissues; in fact, it is the most common GST expressed outside the liver. Based on its overexpression in a majority of human tumor cell lines and prevalence in chemotherapeutic-resistant tumors, GSTP1-1 is thought to play a role in the development of cancer and its potential resistance to drug treatment. Further evidence for this comes from the knowledge that

There is a growing body of evidence supporting the role of GST, particularly GSTP, in cancer development and chemotherapeutic resistance. The link between GSTP and cancer is most obvious in the overexpression of GSTP in many cancers, but it is also supported by the fact that the transformed phenotype of tumor cells is associated with aberrantly regulated kinase signaling pathways and cellular addiction to overexpressed proteins. That most anti-cancer drugs are poor substrates for GSTP indicates that the role of elevated GSTP in many tumor cell lines is not to detoxify the compounds, but must have another purpose; this theory is also given credence by the common finding of GSTP overexpression in tumor cell lines that are not drug resistant.[5]

Assignment 6 (NOT FINAL)

Ideas (TEMPORARY):

• New section: Gene
  • Information about polymorphisms, etc. May not work because of huge variety of superfamilies, classes, isozymes, etc.
• New section: Clinical significance
  • See Gpruett2's suggestions
• New section: History/Discovery
  • How to do this without using primary sources?
• Follow
  these
  guidelines for new sections.

All-new content below! Other changes to GST article documented on user page.

Function

The function of GSTs is dependent upon a steady supply of GSH from the synthetic enzymes

• 
  I made this myself.

Notes