Wikipedia:Articles for deletion/ED1

The following discussion is an archived debate of the proposed deletion of the article below. Please do not modify it. Subsequent comments should be made on the appropriate discussion page (such as the article's talk page or in a deletion review). No further edits should be made to this page.

The result was redirect to CD68. (non-admin closure) CAPTAIN RAJU^(T) 06:38, 17 September 2017 (UTC)[reply]

ED1 (edit | talk | history | protect | delete | links | watch | logs | views) – (View log · Stats)

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While this clone seems to fairly widely-used, I can't find enough information on it to merit an article. It's not clear the subject meets WP:GNG. Perhaps it'd be better for any mention of ED1 to be in the CD68 article. Thoughts? Ajpolino (talk) 23:55, 27 August 2017 (UTC)[reply]

Note: This debate has been included in the list of Science-related deletion discussions. Ajpolino (talk) 23:57, 27 August 2017 (UTC)[reply]

Note: WikiProject Molecular and Cell Biology has been notified of this discussion.Ajpolino (talk) 00:02, 28 August 2017 (UTC) [reply]

Redirect to CD68. If anything passes muster at that article in terms of weight, content could be added there, but I don't see much for that much less it's own article. I'm not seeing anything at first glance, but deletion may be a better option if ED1 is too vague or conflicts with another potential topic title to make a redirect tricky. Kingofaces43 (talk) 00:07, 28 August 2017 (UTC)[reply]

Redirect to CD68. Agree with above. T.Shafee(Evo&Evo)^talk 00:30, 28 August 2017 (UTC)[reply]

• Keep. This subject is covered in depth in numerous serious books and is therefore notable.

• Manual of Stroke Models in Rats spends about a page on ED1 staining.
• Macrophages and Related Cells spends about two pages discussing it (under "Selected Antigens of Rodent and Avian Osteoclasts"). The author singles out the importance of ED1 with; "Earlier studies were limited by the lack of adequate reagents. An exception is the ED1 antigen, which is expressed at high levels in the cytoplasm of both osteoclasts and tissue macrophages."
• Gscholar returns 13,000 results for the search term "ED1 antibody" and 43,000 for just "ED1", including many papers with the term in the title such as Rat macrophage lysosomal membrane antigen recognized by monoclonal antibody ED1 which has the opening sentence "The monoclonal antibody (mAb) ED1 is being used widely as a marker for rat macrophages." SpinningSpark 17:54, 31 August 2017 (UTC)[reply]

Good finds. But my impression is the current thinking is that the antibody called "ED1" is an antibody against rat CD68 (as the two book sources you cite indicate). Can anyone confirm (or deny) that? As such, I think it's best covered there. The only other antibodies we have articles on are antibodies that themselves are therapeutics. Ajpolino (talk) 19:15, 31 August 2017 (UTC)[reply]

I'm not seeing an argument from policy there. My rationale for keeping is WP:N. The argument that we do not have any other non-therapeutic antigen articles (even if true) is a WP:OTHERSTUFF rationale which is widely considered invalid reasoning at AfD. SpinningSpark 20:30, 31 August 2017 (UTC)[reply]

Sorry, to clarify: ED1 is an antibody and the topic of the article. The book passages you posted give a bunch of info about the "ED1 antigen", i.e. the protein to which ED1 binds. That antigen is covered substantially in these books and therefore almost certainly meets WP:GNG. The identify of that antigen is probably CD68 (but I was hoping someone more knowledgeable might know if I'm misunderstanding this). Confusingly, both books sometimes shorten the name "ED1 antigen" to "ED1", even though they're referring to the antigen and not to the antibody. Perhaps the best way to go about this is to make the ED1 article about the "ED1 antigen" and just note that it's the rat homolog of CD68 and that it's so-called because of the name of the antibody that recognizes it? Thoughts? Ajpolino (talk) 21:06, 31 August 2017 (UTC)[reply]

As Kingofaces43 points out, ED1 even with more content is hardly worthy of a stand alone article, thus Redirect is a better choice.Lapabc (talk) 17:39, 12 September 2017 (UTC)[reply]

• Redirect to CD68. The rat ED1 antigen is a synonym for rat CD68 (e.g. 1).--Pontificalibus (talk) 10:08, 10 September 2017 (UTC)[reply]
• Redirect to CD68. I don't think anything can be said to dispute or overturn the points made by SpinningSpark who advocates Keep. I agree that saying only therapeutic antibodies have their own WP page is not valid. Drug companies use WP in a quasi-marketing manner and have their personnel place those WP pages there -- I've witnessed that. Many of those therapeutic antibody pages are useless placeholders, lacking useful information. In any case, the ED1 page suffered from a lack of citations. I just remedied that. With primary citations now in place, the rationale to Delete is reduced. Kingofaces43 points out that this is too minimal for its own article and should be retained if content added. I agree with that too, thus I added content. But with added content it is still too short. If a person was looking to Google for a rat anti-CD68 antibody, an ED1 hit within the WP CD68 page would come up and be very useful, it is not necessary for ED1 to have its own WP page. (As far as policy, if every antigen had its own article we'd have to have tens of thousand of more pages, all fairly minimal and of limited interest.) An ED1 redirect to CD68 meshes well with the "Uses in Pathology" subsection that is already there on the CD68 page. Redirect of the improved ED1 page should be the appropriate action.Lapabc (talk) 17:39, 12 September 2017 (UTC)[reply]

• Note to non-scientists: GScholar is not a great research tool for biomedical sciences, and it is not as useful as one might think for determining WP:N. GScholar yields things like books that have been scanned by Google, blogs that are not peer reviewed, and multiple hits of the same reference (triplicates, quadruplicates, etc.) -- some of that arises from GScholar checking ResearchGate which is yet another multiplier of the same hits. Google took away good Boolean search delimters a long time ago, the lack of which worsens GScholar's utility. Book references are not favored by working scientists because they are derivative in nature -- primary matters -- and they are less accessible and current than electronic journals. As useful as the discussion above was about the number of citations, it would have been more relevant and stronger had the search been from PubMed / PMC / PubChem / NCBI / National Library of Medicine / Web of Science. GScholar returned 13,000 hits for the search term "ED1 antibody." That may be, but that's certainly a bogus result. PubMed turns up 686 hits for "ED1 antibody" and it turns up 688 hits for "ED1 AND (antibody OR monoclonal)." The agreement between those tells you that's the truer number, not 13,000. Sources matter because people misinterpret science all the time, there's a of misinformation out there, science deniers, you name it that Google pulls in but cannot distinguish. For WP to be the source of record, it itself must depend on reliable sources and in science, that means peer-reviewed sources such as those found on PubMed, etc. One hit on PubMed is worth twenty on GScholar. The importance of PubMed cannot be overstated... that's why PMID and PMC and are *standard* parts of WP journal citation templates. Lapabc (talk) 17:39, 12 September 2017 (UTC)[reply]

Just a note that in my vote for clarification since you commented on it. I meant that content should be developed at CD68 before considering assessing whether ED1 has enough muster to have a standalone article. I still don't see evidence for a solid keep and am pretty firm on a redirect at this time. Kingofaces43 (talk) 13:49, 15 September 2017 (UTC)[reply]

BTW, the CD68 page could use some beefing up.Lapabc (talk) 17:39, 12 September 2017 (UTC)[reply]

The above discussion is preserved as an archive of the debate. Please do not modify it. Subsequent comments should be made on the appropriate discussion page (such as the article's talk page or in a deletion review). No further edits should be made to this page.