BH3 Interacting Domain Death Agonist Protein
"BH3 Interacting Domain Death Agonist Protein" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
A member of the Bcl-2 protein family that reversibly binds MEMBRANES. It is a pro-apoptotic protein that is activated by caspase cleavage.
Below are MeSH descriptors whose meaning is more general than "BH3 Interacting Domain Death Agonist Protein".
Below are MeSH descriptors whose meaning is more specific than "BH3 Interacting Domain Death Agonist Protein".
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Below are the most recent publications written about "BH3 Interacting Domain Death Agonist Protein" by people in Profiles.
Multidimensional Control of Cas9 by Evolved RNA Polymerase-Based Biosensors. ACS Chem Biol. 2018 02 16; 13(2):431-437.
An interconnected hierarchical model of cell death regulation by the BCL-2 family. Nat Cell Biol. 2015 Oct; 17(10):1270-81.
The adaptor protein CRK is a pro-apoptotic transducer of endoplasmic reticulum stress. Nat Cell Biol. 2011 Dec 18; 14(1):87-92.
BID, BIM, and PUMA are essential for activation of the BAX- and BAK-dependent cell death program. Science. 2010 Dec 03; 330(6009):1390-3.
Stepwise activation of BAX and BAK by tBID, BIM, and PUMA initiates mitochondrial apoptosis. Mol Cell. 2009 Nov 13; 36(3):487-99.
Regulation of lymphocyte progenitor survival by the proapoptotic activities of Bim and Bid. Proc Natl Acad Sci U S A. 2008 Dec 30; 105(52):20840-5.
Caspase-2 cleavage of BID is a critical apoptotic signal downstream of endoplasmic reticulum stress. Mol Cell Biol. 2008 Jun; 28(12):3943-51.
Intrachromosomal duplications of 22q11 are not a common cause of isolated coloboma and coloboma with other limited features of cat eye syndrome. Am J Med Genet A. 2008 Feb 01; 146A(3):401-4.
Dissection of the BCL-2 family signaling network with stabilized alpha-helices of BCL-2 domains. Methods Enzymol. 2008; 446:387-408.
The intrinsic apoptotic pathway is required for lipopolysaccharide-induced lung endothelial cell death. J Immunol. 2007 Aug 01; 179(3):1834-41.