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Talk:BIN1

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Latest comment: 8 years ago by Rod57 in topic What connection with Alzheimers

Involved in resistance to chemotherapy

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says "the c-MYC oncoprotein decreases production of BIN1, a c-MYC inhibitor. BIN1 usually suppresses an enzyme essential for DNA repair. Thus the sensitivity of cancer cells to cisplatin depends upon BIN1 abundance" Rod57 (talk) 15:06, 26 March 2011 (UTC)Reply

Figure

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The figure showing structure 1bb9 is misleading. This protein is not a single SH3 domain, its a disordered strand with two structural domains BAR/IMD-like and SH3. I suggest it's either removed or a rendering of all NMR states from structure 1MV3 is used instead http://www.rcsb.org/pdb/explore/explore.do?structureId=1MV3. -- MattOates (Ulti) 16:42, 17 July 2012 (UTC)Reply

Also, an almost complete structure of human N-BAR domain of BIN1 is available at http://www.rcsb.org/structure/2FIC

Identify the human isoforms

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Article seems to say there are 10 isoforms in mice. Are they the same in humans ? Which isoform is the tumor suppressor (that acts via IDO) ? Which are found in the CNS, which in muscle ? - Rod57 (talk) 12:04, 31 August 2017 (UTC)Reply

The Entrez source lists 16 isoforms eg :
    • Isoform 1, also called IIa and S11R3-a, binds dynamin, synaptojanin, and clathrin. This isoform is expressed exclusively in the brain and is concentrated in nerve terminals.
    • Isoform 8 is expressed in muscle and localizes to the nucleus.
    • Isoforms 9 and 10 are ubiquitously expressed
    • Isoform 7, also called IIc2 and S1/R3-c, binds dynamin and synaptojanin
    • Isoform 5, also called IIb, binds dynamin, synaptojanin, and endophilin.
    • Isoform 2, also called IId and S1/R3-6, binds dynamin, synaptojanin, and clathrin.
    • Isoform 3, also called IIc1, binds dynamin and synaptojanin.
but not clear which is the tumor suppressor - Rod57 (talk) 12:18, 31 August 2017 (UTC)Reply

What connection with Alzheimers

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4 of the 5 pubmed refs listed in Entrez ref are about Alzheimers. Could summarise here ? - Rod57 (talk) 12:27, 31 August 2017 (UTC)Reply