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![]() | Aryl hydrocarbon receptor received a peer review by Wikipedia editors, which is now archived. It may contain ideas you can use to improve this article. |
Hey so some of the information on this page may be outdated, it says that the identity of the endogenous ligand to this receptor is currently not known. I know of one such ligand, 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE). Here's the article that describes its discovery: http://www.pnas.org/content/early/2010/11/09/1009201107 Here's another article talking about it's use in Nanoparticles: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3396465/ Hopefully someone can go about fixing this issue, I would do it myself but I'm currently doing a project, so I don't have the time. I also don't really wanna go about fixing it and doing it incorrectly. Quite honestly, I really just don't have time to do the citations, but here's the abstract for the first article: An endogenous aryl hydrocarbon receptor ligand acts on dendritic cells and T cells to suppress experimental autoimmune encephalomyelitis The ligand-activated transcription factor aryl hydrocarbon receptor (AHR) participates in the differentiation of FoxP3+ Treg, Tr1 cells, and IL-17–producing T cells (Th17). Most of our understanding on the role of AHR on the FoxP3+ Treg compartment results from studies using the toxic synthetic chemical 2,3,7,8-tetrachlorodibenzo-p-dioxin. Thus, the physiological relevance of AHR signaling on FoxP3+ Treg in vivo is unclear. We studied mice that carry a GFP reporter in the endogenous foxp3 locus and a mutated AHR protein with reduced affinity for its ligands, and found that AHR signaling participates in the differentiation of FoxP3+ Treg in vivo. Moreover, we found that treatment with the endogenous AHR ligand 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) given parenterally or orally induces FoxP3+ Treg that suppress experimental autoimmune encephalomyelitis. ITE acts not only on T cells, but also directly on dendritic cells to induce tolerogenic dendritic cells that support FoxP3+ Treg differentiation in a retinoic acid-dependent manner. Thus, our work demonstrates that the endogenous AHR ligand ITE promotes the induction of active immunologic tolerance by direct effects on dendritic and T cells, and identifies nontoxic endogenous AHR ligands as potential unique compounds for the treatment of autoimmune disorders. — Preceding unsigned comment added by 98.118.113.138 ( talk) 00:05, 7 April 2013 (UTC)
I'm sorry, I have no information, I just seriously could not understand a word of that. And I'm pretty good at Chemistry... and Biology. — riana_dzast a wreak havoc| damage report 06:00, 14 September 2006 (UTC)
Will get started on it shortly. Demantos 17:44, 11 May 2007 (UTC)
UB. Added section pertaining to signaling pathway. Still looking for a good figure to illustrate. Demantos 13:42, 15 May 2007 (UTC) UB. Still cleaning up. Will work on ligands section later. Demantos 15:53, 15 May 2007 (UTC)
UB. Updated the references to the standardized approach. Demantos 15:47, 16 May 2007 (UTC)
UB. All permissions have been obtained for the two images currently displayed. Written permission was obtained from the journals copyright administrator with the understanding that permission would be expressed within the figure legend. Demantos 18:38, 29 May 2007 (UTC)
Please use this tool to keep all references standardized. http://diberri.dyndns.org/wikipedia/templates/ Make sure to check the ADD ref tag box. Demantos 11:40, 29 May 2007 (UTC)
Demantos 18:40, 26 August 2007 (UTC)
Now that I have some more time, I'm still working on the page UB. Demantos 13:39, 7 November 2007 (UTC)
Since I am not sure I can get around to it soon, here are the results of the peer review Demantos ( talk) 15:50, 3 January 2008 (UTC)
A good start: the facts are here and the refs are very thorough. Rewriting (not just punctuation and spelling) will improve the article significantly.
The first paragraph states:
"The Aryl hydrocarbon receptor (AhR or AHR) is a member of the family of basic-helix-loop-helix transcription factors. AhR is a cytosolic transcription factor that is normally inactive, bound to several co-chaperones."
Is it not true that a transcription factor is a PROTEIN that BINDS to a RECEPTOR? If so, then why is the receptor referred to as BEING the transcription factor? It seems that this must be a mistake. 208.54.94.8 ( talk) 17:06, 14 March 2009 (UTC)
=== A receptor binds a LIGAND which can be anything from a protein to a small molecule to a drug, etc. Ligands bind to AHR which then activate the protein and cause it and ARNT to bind DNA causing changes in transcription. Transcription factors bind to DNA. It has been estabilshed for over 30 years that AHR is a transcription factor. This is a basic concept in cell biology, please refer to an appropriate text book. Demantos ( talk)
=== It most certainly is a TF, this paper here describes its binding to cyp1a1 gene: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3396465/ — Preceding unsigned comment added by 98.118.113.138 ( talk) 00:00, 7 April 2013 (UTC)
In a study published on early August 2016, AHR's presence in homo sapiens sapiens has provided this branch a much lesser susceptibility to smoke-induced diseases caused by (fireside) smoke — compared to Neanderthals and the Denisova[n] branch, who did not have AHR. This may have given a genetic advantage to what became the modern human. Article in The Guardian here. - Mardus / talk 11:01, 28 September 2016 (UTC)
All I did was add a space, because I don't know how to ask the question, "Isn't Wikipedia supposed to be for EVERYONE to use?" Anyone who would understand this entry CLEARLY does not need to read Wikipedia for their information, since they've probably already got a PhD in organic chemistry or something. This reads like a journal article or a graduate school textbook and assumes either a VAST amount of pre-existing knowledge or a really hardcore level of motivation (to go after every linked...) 207.138.216.85
![]() | This article is rated B-class on Wikipedia's
content assessment scale. It is of interest to the following WikiProjects: | ||||||||||||||||
|
![]() | Aryl hydrocarbon receptor received a peer review by Wikipedia editors, which is now archived. It may contain ideas you can use to improve this article. |
Hey so some of the information on this page may be outdated, it says that the identity of the endogenous ligand to this receptor is currently not known. I know of one such ligand, 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE). Here's the article that describes its discovery: http://www.pnas.org/content/early/2010/11/09/1009201107 Here's another article talking about it's use in Nanoparticles: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3396465/ Hopefully someone can go about fixing this issue, I would do it myself but I'm currently doing a project, so I don't have the time. I also don't really wanna go about fixing it and doing it incorrectly. Quite honestly, I really just don't have time to do the citations, but here's the abstract for the first article: An endogenous aryl hydrocarbon receptor ligand acts on dendritic cells and T cells to suppress experimental autoimmune encephalomyelitis The ligand-activated transcription factor aryl hydrocarbon receptor (AHR) participates in the differentiation of FoxP3+ Treg, Tr1 cells, and IL-17–producing T cells (Th17). Most of our understanding on the role of AHR on the FoxP3+ Treg compartment results from studies using the toxic synthetic chemical 2,3,7,8-tetrachlorodibenzo-p-dioxin. Thus, the physiological relevance of AHR signaling on FoxP3+ Treg in vivo is unclear. We studied mice that carry a GFP reporter in the endogenous foxp3 locus and a mutated AHR protein with reduced affinity for its ligands, and found that AHR signaling participates in the differentiation of FoxP3+ Treg in vivo. Moreover, we found that treatment with the endogenous AHR ligand 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) given parenterally or orally induces FoxP3+ Treg that suppress experimental autoimmune encephalomyelitis. ITE acts not only on T cells, but also directly on dendritic cells to induce tolerogenic dendritic cells that support FoxP3+ Treg differentiation in a retinoic acid-dependent manner. Thus, our work demonstrates that the endogenous AHR ligand ITE promotes the induction of active immunologic tolerance by direct effects on dendritic and T cells, and identifies nontoxic endogenous AHR ligands as potential unique compounds for the treatment of autoimmune disorders. — Preceding unsigned comment added by 98.118.113.138 ( talk) 00:05, 7 April 2013 (UTC)
I'm sorry, I have no information, I just seriously could not understand a word of that. And I'm pretty good at Chemistry... and Biology. — riana_dzast a wreak havoc| damage report 06:00, 14 September 2006 (UTC)
Will get started on it shortly. Demantos 17:44, 11 May 2007 (UTC)
UB. Added section pertaining to signaling pathway. Still looking for a good figure to illustrate. Demantos 13:42, 15 May 2007 (UTC) UB. Still cleaning up. Will work on ligands section later. Demantos 15:53, 15 May 2007 (UTC)
UB. Updated the references to the standardized approach. Demantos 15:47, 16 May 2007 (UTC)
UB. All permissions have been obtained for the two images currently displayed. Written permission was obtained from the journals copyright administrator with the understanding that permission would be expressed within the figure legend. Demantos 18:38, 29 May 2007 (UTC)
Please use this tool to keep all references standardized. http://diberri.dyndns.org/wikipedia/templates/ Make sure to check the ADD ref tag box. Demantos 11:40, 29 May 2007 (UTC)
Demantos 18:40, 26 August 2007 (UTC)
Now that I have some more time, I'm still working on the page UB. Demantos 13:39, 7 November 2007 (UTC)
Since I am not sure I can get around to it soon, here are the results of the peer review Demantos ( talk) 15:50, 3 January 2008 (UTC)
A good start: the facts are here and the refs are very thorough. Rewriting (not just punctuation and spelling) will improve the article significantly.
The first paragraph states:
"The Aryl hydrocarbon receptor (AhR or AHR) is a member of the family of basic-helix-loop-helix transcription factors. AhR is a cytosolic transcription factor that is normally inactive, bound to several co-chaperones."
Is it not true that a transcription factor is a PROTEIN that BINDS to a RECEPTOR? If so, then why is the receptor referred to as BEING the transcription factor? It seems that this must be a mistake. 208.54.94.8 ( talk) 17:06, 14 March 2009 (UTC)
=== A receptor binds a LIGAND which can be anything from a protein to a small molecule to a drug, etc. Ligands bind to AHR which then activate the protein and cause it and ARNT to bind DNA causing changes in transcription. Transcription factors bind to DNA. It has been estabilshed for over 30 years that AHR is a transcription factor. This is a basic concept in cell biology, please refer to an appropriate text book. Demantos ( talk)
=== It most certainly is a TF, this paper here describes its binding to cyp1a1 gene: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3396465/ — Preceding unsigned comment added by 98.118.113.138 ( talk) 00:00, 7 April 2013 (UTC)
In a study published on early August 2016, AHR's presence in homo sapiens sapiens has provided this branch a much lesser susceptibility to smoke-induced diseases caused by (fireside) smoke — compared to Neanderthals and the Denisova[n] branch, who did not have AHR. This may have given a genetic advantage to what became the modern human. Article in The Guardian here. - Mardus / talk 11:01, 28 September 2016 (UTC)
All I did was add a space, because I don't know how to ask the question, "Isn't Wikipedia supposed to be for EVERYONE to use?" Anyone who would understand this entry CLEARLY does not need to read Wikipedia for their information, since they've probably already got a PhD in organic chemistry or something. This reads like a journal article or a graduate school textbook and assumes either a VAST amount of pre-existing knowledge or a really hardcore level of motivation (to go after every linked...) 207.138.216.85