Talk:Protein kinase B

Origin of Akt name
What does Akt stand for? Danielkueh 07:18, 11 June 2006 (UTC)

Akt is not an abbreviation; it is the name of the gene encoding a particular protein: Akt or Akt1. The name Akt stems from the name of the transforming retrovirus that was first cloned from a translocation into the akt allele; the virus form of the gene was called "v-akt"; the normal, cellular form of Akt, unmutated, was for a short type called "c-akt". Then the normal, unmutated gene was simply called "Akt." Once it was discovered that there are three members to the Akt family, Akt was renamed "Akt1". However, it is usally simply called Akt, whereas the family members "Akt2" and "Akt3" are always referenced with the number. Gacggt 19:10, 4 June 2006 (UTC)

quoted from: http://216.239.59.104/search?q=cache:PiZx_-7x2IIJ:www.scienceforums.net/forum/archive/index.php/t-5226.html+subsequently+designated+by+a+second+small+letter+akt+aa+ab&hl=en&ct=clnk&cd=1

"Following a recent research presentation on Akt, I was asked what Akt stands for....a question to which I had no solid reply...so, here it is...

After an extensive literature search, it turns out the origins of Akt date back to 1928, where J. Furth performed experimental studies on mice that developed spontaneous thymic lymphomas. Mice from three different stocks designated A, R, and S were studied. Stock A was noted to yield many cancers, and inbred families were subsequently designated by a second small letter....Aa, Ab, Ac...thus the Ak strain of mice. Further inbreeding was undertaken with Ak mice at the Rockefeller Institute in 1936, leading to the designation of the AKR mouse strain. In 1977, a transforming retrovirus was isolated from the AKR mouse. This virus was named Akt-8, the "t" representing its transforming capabilities. Ten years later the proviral DNA was cloned and the viral oncogene, v-akt, was discovered. Human homologues Akt1 and Akt2 were later discovered, with gene amplification noted in a human gastric cancer. Akt is now known to regulate many normal cellular functions, and loss of regulatory control has been implicated in many human cancers."

It would be nice to have a good referenced piece of text on this in the article, I guess. (I only made a first attempt, plenty of room for improvement)

As Akt was originally identified as the oncogene in the transforming retrovirus, AKT8.

Thanks a lot for the info. Greatly appreciated. Danielkueh 21:38, 18 June 2006 (UTC)

Involvement of Forkhead Transcription Factors (FoxO and FKHR1), CREB and YAP in Akt survival signalling. I think, the following should be added to this page. Further, Akt can directly inactivate some caspases (most notably Caspase-9).

I am happy to address the question of the naming of akt since I was the one who named the gene. In the early 70s I was a research associate in the laboratory of Wallace P Rowe at the National Institue of Allergy and Infectious Diseases, NIH. The lab research was focused in part on the AKR strain of mice which had been shown by Ludwik Gross to develop a high incidence of spontanous leukemia/lymphoma as a result of viral leukemogenesis. The source of the virus was replication competent endogenous retroviruses which were activated shortly after birth and resulted in increasingly viremic mice as they aged. The mice would eventually die with massively enlarged, malignant thymomas. If you do a pub med search for Wallace P Rowe, you will discover his elegant papers defining the endogenous retroviruses of the AKR mice and the variations in the expressed retroviruses that develop in the premalignant phase. Of particular note is the appearance of xenotropic retrovirues, i.e. viruses with altered tissue tropism that can successfully infect xenogeneic cell lines. Wallace Rowe allowed the research associates latitude in their projects-he encouraged exploration and initiative by those temporarily in the lab as commissioned officers, serving their military duty. I decided to see if I could find directly transforming retroviruses in the virus expressing-malignant tissues of AKR mice. I harvested a series of thymomas, teased apart the cells and overlaid them onto indicator cell lines. One of the cell lines was a mink cell line, in use by the lab to study the xenotropic retroviruses which were then of much interest. I labelled these cultures AKT-#. The ak referred to the akr mice and the t referred to thymoma-the numbering was for each individual thymoma harvested. The eighth culture, AKT-8, produced subtle areas of heaped up cells, or foci of transformed cells, in the mink cell line. These cells were anchorage independent as shown by growth in soft agar, and the transforming activity could be passed with cell free supernatants, indicating a viral etiology. Cloned AKT-8 transformed mink cells were subsequently used to molecularly clone the replication defective provirus using the flanking viral sequences to fish out the transduced cellular sequences with transforming activity. I naturally named this gene akt. The human homologs, akt1 and akt2 were cloned from a human gene library and used to screen a large number of tumor DNAs that I had been collecting (as a medical oncologist, this was not difficult). The first hint that akt might be important for human tumors was the finding of a gastric cancer patient with amplification of the gene. With the collaboration of Joe Testa, then at the University of Maryland, we were able to map akt1 to its chromosomal location. For a variety of reasons, I had to give up my lab effort at that point, but I was happy to see Joe carry the work forward. The original paper is at http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=197531 The cloning paper is at http://www.pnas.org/cgi/reprint/84/14/5034 —Preceding unsigned comment added by Sstaal (talk • contribs) 22:31, 3 June 2008 (UTC)

Related copyleft article
Protein Kinase B by Sebastian Hofbauer is under the CC-BY license. The AGC kinases remain on a list of gene families yet to be sorted and annotated and categorized at Wikipedia. --JWSchmidt (talk) 18:19, 25 August 2009 (UTC)

Much content is specific to akt1
Much of the text, eg under Regulation, seems more about just Akt1 - and should possibly be moved there ? Rod57 (talk) 08:53, 28 February 2011 (UTC)

How do you say AKT?
Is it pronounced like "act" or as "Ay Kay Tee" or "Ack Tee" or what? — Preceding unsigned comment added by 216.66.5.47 (talk) 16:16, 23 April 2014 (UTC)

In my lab, everyone calls it "ay kay tee" — Preceding unsigned comment added by 2.31.29.235 (talk) 02:45, 2 August 2014 (UTC)

Family
The first chapter is about the 3 members of the Akt family, but then, all references are about Akt like it's a single protein.

If Akt1 and Akt2 have different effects on main threads (protein synthesis or glycemia), they should have different regulation or even different pathways, no ? — Preceding unsigned comment added by 164.2.255.244 (talk) 15:02, 8 December 2015 (UTC)

Merger proposal
Formal request has been received to merge content from the article Protein kinase B that is specific to AKT1 to AKT1; dated: September 2017. Discuss here. Richard3120 (talk) 15:39, 15 October 2017 (UTC)
 * Merge should proceed as there are no objections. GenQuest  "Talk to Me" 21:13, 1 June 2018 (UTC)
 * Support Since there is an article for AKT1, that's where the information specific to it should be. So agreed. Take most of the content from PKB but leave a brief paragraph about AKT1 in the context of PKB. Jamgoodman (talk) 19:51, 29 May 2019 (UTC)
 * WikiProject Molecular Biology has been notified to help effect moving the content to the right place. Felix QW (talk) 15:13, 27 May 2023 (UTC)