Wednesday, February 13, 2013

GENES OF CELLULAR DEATH.

1.  BIM or BCL2-L11

BCL2L11

From Wikipedia, the free encyclopedia
Jump to: navigation, search
BCL2-like 11 (apoptosis facilitator)

Rendering based on PDB 2K7W.
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols BCL2L11; BAM; BIM; BOD
External IDs OMIM603827 MGI1197519 HomoloGene7643 ChEMBL: 5777 GeneCards: BCL2L11 Gene
RNA expression pattern
PBB GE BCL2L11 208536 s at tn.png
PBB GE BCL2L11 222343 at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 10018 12125
Ensembl ENSG00000153094 ENSMUSG00000027381
UniProt O43521 O54918
RefSeq (mRNA) NM_001204106.1 NM_009754.3
RefSeq (protein) NP_001191035.1 NP_033884.1
Location (UCSC) Chr 2:
111.88 – 111.92 Mb
Chr 2:
128.13 – 128.16 Mb

PubMed search [1] [2]
Bcl-2-like protein 11 is a protein that in humans is encoded by the BCL2L11 gene.[1][2]
The protein encoded by this gene belongs to the BCL-2 protein family. BCL-2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. The protein encoded by this gene contains a Bcl-2 homology domain 3 (BH3). It has been shown to interact with other members of the BCL-2 protein family, including BCL2, BCL2L1/BCL-X(L), and MCL1, and to act as an apoptotic activator. The expression of this gene can be induced by nerve growth factor (NGF), as well as by the forkhead transcription factor FKHR-L1, which suggests a role of this gene in neuronal and lymphocyte apoptosis. Transgenic studies of the mouse counterpart suggested that this gene functions as an essential initiator of apoptosis in thymocyte-negative selection. Several alternatively spliced transcript variants of this gene have been identified.[3]
Interactions BCL2L11 has been shown to interact with DYNLL1,[4][5] MCL1,[1][6][7] BCL2-like 1,[1][2][6][8] BCL2L2[1][2] and Bcl-2.[1][2][6]
======================================================================================== 
COMMENTS:

BIM IS IN FACT CONSIDERED A MEMBER OF THE BCL FAMILY ONLY BECAUSE IT HAS A BH3
IN FACT AS STATED IT INITIATES APOPTOSIS.  IT ACTUALLY BINDS BCL FAMILY MEMBER AND DESACTIVATES THEM OR VICE VERSA.  MEANING THE MORE IT IT IS ATTACHED TO OTHER MEMBERS IF THERE IS ENOUGH BCL2 LEFT THE CELL IS PROTECTED.  BUT IF NOT, THE CELL IS OPEN TO DEATH.   IT IS DEGRADED THROUGH THE PROTEASOME.  IT IS THEREFORE UPREGULATED BY VELCADE.  TAXANE DOWNREGULATES BIM THEREFORE BIM IS PART OF TAXANE INEFFICIENCY LEADING RESEARCHER TO BELIEVE TO THE VALUE OF TAXANE VELCADE COMBINATION.

LEVEL OF BIM COULD THEREFORE BE A SURROGATE FOR MEASUREMENT ON WHETHER DRUGS ARE ADDITIVE  OR COUNTERPRODUCTIVE IN LABORATORY WHEN IT COMES TO THE CURE.

2. BID


3.BAD
4.NOXA
5.PUMA (HIDING BEHIND FOXO3 AND THE MTOR ALREADY DISCUSSED)
6.BH3 UPREGULATION
7.DEPRESSION OF Bcl-XL
8.BAX
9.Fas PLUS FASL FORM DISC
10.Death Receptor

No comments: