Wikipedia talk:WikiProject Molecular Biology/Molecular and Cell Biology/Archive 11

@Shyamal, Boghog, Seppi333, and UnitedStatesian: I have pinged all of you as you are marked as active participants under Wikiproject Directory tool.

I generally think the proposed merger would be beneficial as most if not all of the involved projects are well below critical mass. (It is a bit depressing to learn that there are only 4 active

WT:MCB editors). Boghog (talk

) 16:05, 10 June 2019 (UTC)

Merger complete! See the new unified talkpage. All talkpage archives should be clearly visible and searchable and the new unified WikiProject page is almost complete. T.Shafee(Evo&Evo)^talk 12:25, 16 June 2019 (UTC)

There's a discussion about a possible User Group for STEM over at Meta:Talk:STEM_Wiki_User_Group. The idea would be to help coordinate, collaborate and network cross-subject, cross-wiki and cross-language to share experience and resources that may be valuable to the relevant wikiprojects. Current discussion includes preferred scope and structure. T.Shafee(Evo&Evo)^talk 03:04, 26 May 2019 (UTC)

Hello everyone, i am the author of the DNA replication image give or take i made this image arround 2007, i have been asked to modify it to incorporate all the comments and corrections made on the discussion page plus someone left the following request on the Graphics lab on commons:

Pol epsilon should be on the leading strand and attached to the helicase (which should have a ring structure). Pol delta should be on the lagging strand. Pol delta might have some role in leading strand replication (still debated to which extend), but is mostly responsible for lagging strand replication. See also

)

Now I am an illustrator and by no means expert in this subject so i would really appreciate if someone with the appropriate knowledge could have a look on this Sketch. it isnt yet on its final form but the elements are in the relative position i am hoping them to have (all marked with ? would need some reassuring). also there is like a ton of questions i would really want to have answer if that is ok:

• I have been told that the polymerase that works on the leading strand is attached to the helicase. if so, where do the SSBs (single stranded binding proteins) connect on that side of the fork? also i have seen other diagrams with this polymerase hugging the lagging strand instead sso whicone would be correct?
• i made the sliding clamp on the polymerase seem part of the same body, i am aware it is a completely different enzyme is just i thought it would show they both work together and also gives the drawing some directionality which seems to be important in this subject. is this ok?
• i am very confused about which polymerase is what greek letter of pol. on the sketch i have made my best guess but i still not sure which is which. Also would it be a problem if a place several polymerases working on different sections of the lagging strand? at the moment the same primase, and polymerase must go round and round backwards to do the job.
• on the last image i was asked at least once a month to change the 3'5' notations on the diagram. i have made a little color hook on the primers to show where the 3' end of it would be, and made a image section to explain here is where the polymerase attaches to start working. would this be helpfull or do you think it will make things more confusing?
• is it practical to add the Telomerase in the diagram? i am not even sure if it would attach there, would you find it more useful or should i leave it out?
• because of space resstrains i placed the RNAse at the same spot than the DNA polymerase that repairs the gap. is this understandable or would they need their own gap?
• In many images i have fished out online (excluding those based on my own image) i have found often that enzymes are much bigger than what i have show, and i dont mind that becouse more than scale i am more interested in showing function, but it does worry when i see images like this one where the single strand make strange loops.. is there anything about this i should be aware of?

if you would be so kind to answer my questions i could at least have some degree of confidence in remaking the image in a better more accurate state. 大诺史 was kind to offer this article as reference [10]. I look forward to your feedback. and thank you for your time -LadyofHats (talk) 18:58, 5 June 2019 (UTC)

The articles pre-replication complex, minichromosome maintenance, and origin recognition complex can use some better images for the protein structures in light of the not-so-recent publications of EM structures. My computer and my brain are currently too messed up to sort out the PyMol or whatever rendering thing, so would anyone please render some views (two will do: front and top) for PDB ID 5v8f (pre-RC OCCM), 3JA8 (MCM; 5UDB will do too), and 4XGC (ORC; 5UDB will do too)? --Artoria2e5 🌉 23:48, 23 June 2019 (UTC)

Gene symbol link targets that don't include the words "protein", "proteins", "gene" or "genes"

So, below is what my algorithm found.

If the mistargeted gene symbol isn't a redirect, it's listed as en:PAGENAME on that line.

If the term is a redirect, the format below is en:REDIRECT → en:PAGENAME. Seppi333 (Insert 2¢) 05:15, 26 November 2019 (UTC)

I'm not sure how to address this. For each gene symbol below that no relevant article exists, should we just create a DAB pages with redlinks to SYMBOL (gene) listed on it? A lot of the symbols below should clearly link to disambiguation page. Seppi333 (Insert 2¢)

Actually, I think it would make sense for me to just pipe the links for the gene symbols to SYMBOL (gene) for now and maybe get some assistance from WP:WikiProject Disambiguation on this to address the DAB issues. This approach doesn't work for the enzyme pages though since, like Boghog mentioned: It makes sense to merge enzyme EC and gene Wiki articles if and only if there is a one-to-one correspondence between EC number and HUGO gene symbol. I could really use some help going through the enzyme page links below to see whether or not the gene symbol should redirect there or to SYMBOL (gene). I intend to deal with all the others myself using the algorithm I've described below. Seppi333 (Insert 2¢) 09:39, 26 November 2019 (UTC)

Assistance needed with enzyme entries 7, 129, and 179. The issue is described on the line for that entry. Addendum: I'm just going to ignore the issues and pipe the links to the parenthetically disambiguated gene symbol for the 3 entries. If anyone has a better solution based upon what I wrote below, feel free to chime in. I'm going to leave the gene symbols for the other enzymes in this list unpiped since they're the correct targets. Seppi333 (Insert 2¢) 05:53, 27 November 2019 (UTC)

Nvm. It's readily apparent to me what to do now. FYI: I've been merging and redirecting a number of duplicate WP articles and moving sitelinks from protein pages to gene pages on WD when a 1:1 correspondence exists between them. Seppi333 (Insert 2¢) 00:18, 30 November 2019 (UTC)

Note to self: Still need to address the

HADH link in the list below and in the list of human protein-coding genes table. Seppi333 (Insert 2¢

) 00:20, 30 November 2019 (UTC)

New RFBA since I now have the data that I was going to program this algorithm to obtain – Wikipedia:Bots/Requests for approval/Seppi333Bot 2. Haven't processed the query results yet, but I expect it'll permit creation of about ~2000 gene symbol redirects. Seppi333 (Insert 2¢) 01:29, 20 December 2019 (UTC)

Prime editing has hit the mainstream press, with lots of hyperbole about its potential, in spite of it still being at the laboratory proof of concept stage. I've created a stub article for it; can knowledgable people please help improve the article? -- The Anome (talk) 09:33, 22 October 2019 (UTC)

Hello and greetings from the maintainers of the WP 1.0 Bot! As you may or may not know, we are currently involved in an overhaul of the bot, in order to make it more modern and maintainable. As part of this process, we will be rewriting the web tool that is part of the project. You might have noticed this tool if you click through the links on the project assessment summary tables.

We'd like to collect information on how the current tool is used by....you! How do you yourself and the other maintainers of your project use the web tool? Which of its features do you need? How frequently do you use these features? And what features is the tool missing that would be useful to you? We have collected all of these questions at this Google form where you can leave your response. Walkerma (talk) 04:24, 27 October 2019 (UTC)

The following discussion may be of interest to this project: Wikipedia_talk:WikiProject_Medicine#MEDRS_sourcing_required_for_non-biomedical_information. --Signimu (talk) 17:50, 1 November 2019 (UTC)

I wrote the bot script yesterday morning and it's been operating since then. Pending approval of my bot and validating the links as mentioned in the section below, I'll move those tables to the mainspace. Seppi333 (Insert 2¢) 18:16, 6 November 2019 (UTC)

I haven't programmed an algorithm to detect the mistargeted links in the wikitables yet (there's only a few dozen mistargeted links in both tables based upon their rate of occurrence in the few thousand links I've followed); however, in order to follow-up on the discussion in the request for approval page, I moved the tables to the mainspace at List of human protein-coding genes 1 and List of human protein-coding genes 2. If anyone has any feedback/suggestions pertaining to the page layout or the tables themselves, please let me know. Seppi333 (Insert 2¢) 02:33, 24 November 2019 (UTC)

My assumption is that you are creating this table so that you can quickly find GeneWiki articles for specific genes. Sometime ago, I had a bot add a redirect "<HUGO gene sybmol> (gene)" for every GeneWiki article (see BFA:BogBot_3). This provided an ambiguous way of locating GeneWiki article. These redirects should probably be updated. As you point out, there are limitations to the size of pages. Why not rely on Wikipedia's search engine instead? Boghog (talk) 11:05, 24 November 2019 (UTC)

My primary personal motivation for adding that table was mostly just curiosity and a desire to be able to visualize the completeness of different gene groups in the GeneWiki and the completeness of our coverage of protein-coding genes as a whole (i.e., compare # red vs # blue links). Due to how fragmented the GeneWiki is (mostly due to PBB's bugs), I don't think I'd ever use those tables to navigate to a specific gene. It could serve as a centralized internal navigation page for protein-coding GeneWiki pages, but all the articles on protein coding-genes that are located at an obscure pagename (i.e., gene or protein alias) w/o redirects from the gene symbol would need to be located and moved to the right place first. I've found and corrected a few of those in the past, but I can't remember the pagenames off the top of my head.

I added it to the article space because several non-editors I asked thought it would be interesting and/or useful. Also, if you hadn't disambiguated the gene pages that way, it'd have taken me a lot longer to disambiguate those links, so ... Thank you. Seppi333 (Insert 2¢) 20:57, 25 November 2019 (UTC)

I forgot to add, I broke this list up into 4 pages due to how large they were as 2 relative to those list in Special:LongPages. Now, 3 of them are in the top 10 largest mainspace pages. Seppi333 (Insert 2¢) 21:19, 25 November 2019 (UTC)

Is there a specific reason given in

WP:DEL-REASON that the PROD is based on? If not, then dePROD it would be since it is an inappropriate use of PROD. In fact, is there any discussion where being withdrawn in HGNC is a valid reason for deletion? As far as I can see, it has not disappeared since it is still in other databases, merely that HGNC chose not to list it. If it gets deProdded, you start a AfD so that such deletion can be discussed. Hzh (talk

) 15:46, 30 November 2019 (UTC)

Don’t care enough to bother. FWIW, look up what “withdrawn entry” actually means as a status label. Seppi333 (Insert 2¢) 00:48, 1 December 2019 (UTC)

It is irrelevant for PROD, because notability of an article may still exist even if the object of the article no longer exists. For example, you can still have an article about

phlogiston even if it has been shown not to exist. Such articles need a proper discussion to determine if they still have a reason to exist. The discussion can be wide-ranging to cover all entries that HGNC had withdrawn so that all such articles can be deleted unless there are specific reasons not to. Hzh (talk

) 02:15, 1 December 2019 (UTC)

@Hzh: There’s exactly 1 30-year old publication about it listed in databases, 0 papers on pubmed indexed to the symbol [21] and 0 papers indexed to “eye color 1” [22]. I assumed this was evident from the link in reason I left in the prod template, but perhaps that’s not the case. If you feel a single primary source establishes notability for the topic despite the fact that its existence is in doubt, fine. Seems odd to me. Don’t really feel like arguing this though, so we’ll keep it. Seppi333 (Insert 2¢) 03:06, 1 December 2019 (UTC)

The original paper is still cited in 2014 - [23], so it hasn't disappeared. It seems that HGNC chose not to maintain symbols for phenotypes, which may be the reason for its withdrawal rather than it not existing (its locus is phenotype only rather than a gene product), so this discussion may be going in completely the wrong direction. Hzh (talk) 04:09, 1 December 2019 (UTC)

Moved to

WT:MOLBIO § Cathelicidin

 – Per request. Seppi333 (Insert 2¢

) 06:22, 30 November 2019 (UTC)

On the one hand, this bot had some problematic bugs prior to being blocked; I've personally had to merge/regarget dozens of erroneous pages it created. As far as I am aware, it correctly wrote page content, but sometimes got the page name wrong, created a duplicate entry, and/or created a redirect to the wrong pagename.

On the other hand, subsequent to identifying the 215 mistargeted links in

1. The biogps.org website still appears to support the user-activated feature for creating gene articles via ProteinBoxBot, although the bot obviously can't edit right now so it doesn't work.
2. The bot is somewhat error-prone, so a human needs to verify that there are no problems with the pages it creates.
3. Abandoned pages in the draft namespace are eventually deleted and there is obviously no harm at all in the creation of duplicate or mistitled entries in that namespace.

A relatively simple solution to keeping my brain intact, my wall stain-free, and PBB's bugs in check is to modify the bot code so that it writes gene articles to the corresponding pagename in the draft namespace upon user activation at biogps.org or via other means. Whoever activates the bot would then have the option of moving the created page to the mainspace. Since it would necessarily be the responsibility of the person who moves that draft to the mainspace to validate the page, this should effectively address all the past concerns about this bot.

@

For a much less self-centric motivation: WP has ~11500 bluelinked protein-coding gene symbols and ~8500 redlinked ones. PBB created ~9400 articles (non-redirect, still live pages) since it was created. Given its original purpose, I suspect that the majority of the 9400 pages PBB created are the articles or targets of the redirects located at those 11500 symbols. So, in spite of its bugs, Wikipedia needs algorithms like PBB if we’re ever going to finish creating the entries for the other half of the exome. Seppi333 (Insert 2¢) 04:12, 2 December 2019 (UTC)

There are many of genes whose function has not yet determined and have not been mentioned in reliable secondary sources, hence these genes fail

WP:NOTABILITY

requirements. Articles for these gene should probably not be created until something more about their function is known.

While the ProteinBoxBot has been blocked, the BioGPS tool still is able to produce the text for a Gene Wiki page (see for example Genereport ALLC and press "Toggle Stub Code"). This can be copied and pasted to create a new article. Boghog (talk) 04:39, 2 December 2019 (UTC)

There are many of genes whose function has not yet determined and have not been mentioned in reliable secondary sources, hence these genes fail

WP:NOTABILITY

requirements I’m well aware.

There’s also protein-coding genes that haven’t even been identified yet. I’m not advocating the overnight creation of 8500 articles. I’m saying we need PBB to even attempt it over time. Addendum: will look into what you linked when back on a computer; using mobile right now. Seppi333 (Insert 2¢) 04:50, 2 December 2019 (UTC)

Hmm. Wasn't aware of that. Well, I'm not sure why we haven't been listing that tool on

WP:MOLBIO, but we're going to now. That tool deals with almost all the BS I mentioned by fully automating the creation of the article's source code, provided there's a non-empty summary field in the NCBI gene entry for the corresponding gene in Homo sapiens; the only manual work required is the adding project templates and creating the sitelink. Seppi333 (Insert 2¢

) 05:31, 2 December 2019 (UTC)

@Andrew Su: Ty for creating that; makes all the work ahead of me seem much more bearable now. Seppi333 (Insert 2¢) 06:14, 2 December 2019 (UTC)

@Seppi333 and Boghog: Great! Glad that work-around is working out for you... Best, Andrew Su (talk) 16:39, 2 December 2019 (UTC)

Section reflist

I have nominated

So, this is something I wondered about years ago, but it's time for me to raise it again. What are the thoughts of people about writing articles like List of human Nrf2 targets (i.e lists of genes that are regulated by a given transcription factor)? They might be of interest to readers, but I don't know what kind of issues they might do. Jo-Jo Eumerus (talk) 19:01, 17 April 2020 (UTC)

I assume you mean target genes of a given transcription factor (e.g., NFE2L2#Target_genes). My worry is that the underlying experimental data for example from ChIP sequencing maybe somewhat unreliable. Are there databases that list such information that include a reliability score? Also this could be quite messy. Regulated genes may be context specific (regulated in some tissues and not others). Boghog (talk) 19:53, 17 April 2020 (UTC)

@Boghog: To be honest, I was thinking of using more focused sources (publications discussing one or a few particular target genes) rather than databases. Great lists with little supplemental information for each item are something I don't think makes for great sourcing. Jo-Jo Eumerus (talk) 08:44, 29 April 2020 (UTC)

@Jo-Jo Eumerus: Yes, I agree it would be much better to base these lists on review articles where there are multiple lines of evidence supporting a given target gene. This would be better than a reliability score reported in a database. Boghog (talk) 13:27, 29 April 2020 (UTC)

Somehow I don't tink there'll be many such reviews. At best, you'd find a paper saying "previous studies[1][2] indicate that HMOX1 is a Nrf2 target gene" which technically satisfies

WP:SECONDARY requirements. Jo-Jo Eumerus (talk

) 13:35, 29 April 2020 (UTC)

According to UniProt, the canonical protein isoform of TNXB has a length of 4244 AA. These frameshifts both occur at glycine residue 362, are >90% truncated relative to the wild-type tenascin-X protein, and they lack nearly all functional domains on the wild-type protein (https://www.uniprot.org/uniprot/P22105#family_and_domains). Complete deficiency in this gene is supposedly highly penetrant for clEDS, but it's somehow only partially penetrant in my brother's case; it's definitely not because one of these proteins is expressed, partially folded, and somehow functional on the sequence preceding the mutation though.

In any event, I'm finding it pretty hard to grasp how this is possible in terms of genetic inheritance unless this involved some abnormal form of inheritance; it just seems unfathomably unlikely that both my parents carry nearly identical frameshift mutations which haven't been previously reported and that both involve an A>G mutation and affect the same protein residue. Sequencing them both would obviously determine if that's the case, but TNXB sequencing is prone to errors due to significant pseudogene interference from TNXA and I don't think it's likely to happen anyway.

Could this arise from uniparental disomy? Or is there another abnormal mode of inheritance that might give rise to seeing mutations like this? I'm just a bit baffled due to my ignorance in this area. Facepalm Seppi333 (Insert 2¢) 12:40, 20 May 2020 (UTC)

Previous thread

Hi Seppi, I'm not a clinician, but I can offer a few thoughts to guide your research:

• It's not clear to me whether your brother's alleles are identical. If so, uniparental isodisomy could certainly be the explanation.
• Chimerism
  in parent or offspring can also explain anomalous inheritance, or inheritance that seems inconsistent with phenotypes.
• These are both rare. Incomplete penetrance and variable expressivity are far more common and mundane, so probably more likely, though I haven't looked into the specifics of TNXB.
• I think you're misunderstanding the word "penetrance". If we say that a genotype is, for example, "70% penetrant", it means 70% of people with that genotype will have at least one detectable aspect of the associated phenotype, however mild; the other 30% have no detectable phenotype. It's a population thing. In a given individual, a genotype is either penetrant or it's not. Mild vs. severe cases are an example of variable expressivity. (Sorry if this sounds pedantic, but I can't tell whether you're misunderstanding something you've read.)
• You mentioned in the previous thread that frameshifts produce non-functional proteins. In fact, frameshifts in eukaryotes often/usually lead to no protein at all, as the mRNAs are destroyed by nonsense-mediated decay.
• In principle, an early frameshift could be compatible with production of at least some functional protein if (1) the mutation is excluded from at least some transcripts by alternative splicing, or (2) an alternative transcription start site (anyone want to blue that red?) leads to mRNAs with a start codon that comes after the mutation. I haven't checked whether enough is known about TNXB to support or rule out those possibilities.
• A frameshift can also be functionally "reversed" by another nearby frameshift. For example, if there's a single base-pair insertion early in the gene, and a single base-pair deletion several codons away, you'd end up with several gobbledygook codons in between. But as long as the gobbledygook did not include a stop codon, the overall protein could still be functional.

In other news, is this seriously only the third thread on this page all year?? I'm glad we merged. Adrian J. Hunter^{(talk•contribs)} 06:43, 21 May 2020 (UTC)

I haven’t visualized my brother’s genome on chromosome 6 because TNXB is located in the major histocompatibility complex and I’m pretty sure my brother’s short-read assembly was generated from alignment-based methods following GATK.

The MHC can’t be resolved by that approach. Short of Sanger sequencing the entire region, the only other way to resolve it is generating contigs from de novo assembly that span most or all of that region. Since de novo hybrid genome assembly will produce longer contigs, that’s what I’ve been working on since I posted this thread. After about 15-20 hours of research and a lot of data wrangling, I started running the Wengan-D assembler today. It takes 1000 cpu hours and requires >600 GB of RAM (not hard disk space) to run, but it’ll give me the most contiguous high-quality assembly of my brother’s datasets that current technology can provide. Also, the paper published about it used the WenganD assembler on same DNA sequencing technology (Illumina NovaSeq and ONT PromethION) with approximately the same level of coverage as my brother’s datasets to almost completely resolve MHC regions I and II in ~4-5 contigs (see fig 2 [24]). MHC region IIi, where TNXB is located, spans 700 kB, but I expect this assembly to have an NG50 in the 8-20 Mb range, so I will likely have that whole region fully resolved on a single contig. In about 5 days, the assembly will be done; I’ll need to compute the validation stats for the assembly, computationally resolve the haplotigs into a diploid assembly, and then align it to a reference genome before I can visualize it. At that point, I’ll be able to see whether or not there’s a lot of unusual sequence similarity on chromosome 6 which is characteristic of isodisomy.

Regarding “penetrance”, in this particular context it’s a bit hard for me, since the biallelic genotype is diagnostic for clEDS and the monoallelic genotype is often associated with hEDS. Given that the biallelic genotype has never been reported to cause the milder hEDS and that these are clinically distict phenotypes, it’s hard for me to describe correctly. I get that penetrance is something-or-nothing, but the variable expressivity of the clinical phenotypes of clEDS and hEDS - based upon the diagnostic criteria alone - do not overlap. That’s why I described it in that manner.

Re: nonsense-mediated decay - that’s useful to know, thanks. Seppi333 (Insert 2¢) 22:05, 24 May 2020 (UTC)

Edit: just to clarify, the aspect of clEDS which is just entirely unlike my brother's phenotype is skin involvement. He has no overt skin abnormalities, although something might be noticeable in a histological examination of his skin tissue (this hasn't been conducted). Seppi333 (Insert 2¢) 22:43, 24 May 2020 (UTC)

Edit: When I say "unusual sequence similarity", I'm mainly referring to variant similarity, not whether or not the wild-type sequences are the same; my brother is obviously human. Seppi333 (Insert 2¢) 22:49, 24 May 2020 (UTC)

Hello guys and gals,

Can someone get the archiving fixed on Talk:Archaea, please? It is getting long and has posts going back to 2014. Thanks, Galendalia Talk to me ^{CVU Graduate} 13:58, 30 May 2020 (UTC)

 Fixed I hope. Boghog (talk) 15:08, 30 May 2020 (UTC)

LOL @Boghog: I know that feeling! 70 iterations later. Thanks! Galendalia Talk to me ^{CVU Graduate} 15:19, 30 May 2020 (UTC)

I have nominated

There have been a lot of small edits from brand new users to this article. Just about every red name in the edit history has made exactly that one edit. I thought they were all one person, but it looks like I was wrong. A lot of them are unsourced with no edit summary and change around the meaning of the article. I don't have the subject knowledge to say if these are vandalism or plausible though, perhaps someone on this WikiProject can take a look through edits such as these? 1 2 3 4 5 For example, I can vaguely say that the first edit I linked is probably incorrect...? But I'm far from certain. (Those 5 are just an example, there are many more in the history, some reverted, some accepted) Leijurv (talk) 20:48, 8 July 2020 (UTC)

Ugh, what a mess. I've never seen anything like this! All five diffs you linked are erroneous. This goes back to at least 2018... I'm going through the article history, looking to revert to stable version. Adrian J. Hunter^{(talk•contribs)} 01:12, 9 July 2020 (UTC)

The first of the bad-faith edits seems to have been this one from February 2018. Too bad for anyone who's relied on our article since then. I've reverted to the version immediately before that. There are some substantive good-faith additions in the intervening versions; if no-one beats me to it, I'll restore those manually later on. Thanks for posting about this, Leijurv. Adrian J. Hunter^{(talk•contribs)} 01:32, 9 July 2020 (UTC)

Sure thing! I just saw your reinstating of the constructive edits, wow! Thank you for sorting out what's correct and what wasn't, going back over two years. :) Leijurv (talk) 18:52, 13 July 2020 (UTC)

Talk:G4 EA H1N1#Proposal: Redirect to main H1N1 article SandyGeorgia (Talk) 04:46, 12 July 2020 (UTC)

Well spotted. I've replied over at Talk:Cis-regulatory_element to help keep the record together. T.Shafee(Evo&Evo)^talk 11:07, 25 July 2020 (UTC)

It seems there's consensus. Could someone close the merger discussion over there so we can get it done? Chiswick Chap (talk) 09:57, 3 August 2020 (UTC)

The articles https://en.wikipedia.org/wiki/Cell_communication_(biology) and https://en.wikipedia.org/wiki/Cellular_communication_(biology) should be merged. RIT RAJARSHI (talk) 09:34, 30 July 2020 (UTC)

It looks like many of the Wikiproject Molecular Cell biology articles lacking details and remaining unimproved for years to decades. Recently I noticed an article whose title does not match with its content (https://en.wikipedia.org/wiki/Membrane_topology). Looks like there are scope of lot of improvements in many of the articles, which are not happening. Is there a deficit or reduction of contributors? Also is there a general reduction of wikipedia activities? How can we again increase activity in Wikipedia? With best wishes for Wikipedia. Thanks in advance. RIT RAJARSHI (talk) 09:38, 30 July 2020 (UTC)

MCB is very broad subject with a large number of stubs and many potential articles still unwritten. At the same time, participation in MCB and in Wikipedia as a whole as dropped. Given the breadth of the subject and the declining number of editors, the best we can probably hope for is to maintain high priority articles and to create a few new articles on hot emerging topics. Student editors can and do help, but they also create a significant amount of work for the regulars. There has been a lot of discussion on increasing participation, but few results. Boghog (talk) 10:43, 30 July 2020 (UTC)

Let us be realistic. Apart from the occasional generous contributions by students and industry, and lots of imported articles (from InterPro, TCDB, EC), this was always mostly an endeavour for amateurs, and molbio has much less amateurs because any halfway knowledgeable molbio amateur gets a good job that completely grabs their time. Personally I have come to the conclusion that, once the basic concepts are done in WP, most molbio facts can be expressed by Wikidata statements. Together with automatic translation this will be the only way to spread the knowledge in all languages. Because, let's face it, en-WP is still much more complete than any other language WP. --SCIdude (talk) 09:45, 3 August 2020 (UTC)

While I think WikiData is useful, I think you are putting the cart before the horse. Without corresponding Wikipedia content, WikiData has very limited value. I also think you are grossly underestimating the contribution of both professionals an amateurs. For a recent high quality contribution, see for example Holocentric chromosome. The intention of Gene Wiki was to provide seed articles that human editors would later expand. Granted, most of these articles have not been expanded, but at least a few like Reelin that have been significantly expanded by knowledgable editors. You are correct that students get professional jobs (and start families, etc.) therefore have less time to devote to Wikipedia. However there are also cases of retired professionals who now have more time to devote to Wikipedia. Boghog (talk) 20:13, 3 August 2020 (UTC)

Judging by incoming articles at NOP and AfC, there seem to be many people, a good number of them ptobably students, who like to do such articles. What we realy need, as IT RAJARSHI indicated, are people to revise the older ones. That may not as much excitement and prestige, but its can make for good group projects. DGG ( talk ) 09:44, 12 October 2020 (UTC)

I have nominated

User:Ajpolino has raised a number of important issues at the featured article review that would require a fairly extensive effort to fix. User:Hanif Al Husaini and I have worked to add citations and I can further update the citations with the most recent editions of cell biology text books. Are there any volunteers to help out with the other issues that Ajpolino raised? I will try to address some of these other problems, but I have fairly limited time to devote to this. Boghog (talk) 10:24, 24 October 2020 (UTC)

In retrospect, it does seem rather inappropriate for me to have posted what DGG deleted in this section, so I wanted to apologize to those here (re this discussion: User talk:Seppi333#October 2020). My bad. I hope everyone can forgive my lack of forethought and stupidity for committing a faux pas. Seppi333 (Insert 2¢) 07:45, 15 October 2020 (UTC)

Yes I could be

Hi, thanks for your message. The intention of

ADRB3 according to the GPCRdb, signals primarily through Gs. This is already mentioned in the Mechanism of action section. Based on the data in GPCRdb, we could add a short mechanism of action section for each of the GPCRs. Boghog (talk

) 10:09, 13 October 2020 (UTC)

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