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Bcl-2-associated death promoter

Bcl-2-associated death promoter

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BAD
Available structures
PDB Ortholog search: PDBe RCSB
Identifiers
Aliases BAD, BBC2, BCL2L8, BCL2 associated agonist of cell death
External IDs OMIM: 603167 MGI: 1096330 HomoloGene: 3189 GeneCards: BAD
Orthologs
Species Human Mouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_032989
NM_004322

NM_007522
NM_001285453

RefSeq (protein)

NP_004313
NP_116784

NP_001272382
NP_031548

Location (UCSC) Chr 11: 64.27 – 64.28 Mb Chr 19: 6.92 – 6.93 Mb
PubMed search
Wikidata
View/Edit Human View/Edit Mouse
Pro-apoptotic Bcl-2 protein, BAD
PDB 1g5j EBI.jpg
complex of bcl-xl with peptide from bad
Identifiers
Symbol Bcl-2_BAD
Pfam PF10514
InterPro IPR018868
Available protein structures:
Pfam   structures / ECOD  
PDB RCSB PDB; PDBe; PDBj
PDBsum structure summary

The BCL2 associated agonist of cell death (BAD) protein is a pro-apoptotic member of the Bcl-2 gene family which is involved in initiating apoptosis. BAD is a member of the BH3-only family, a subfamily of the Bcl-2 family. It does not contain a C-terminal transmembrane domain for outer mitochondrial membrane and nuclear envelope targeting, unlike most other members of the Bcl-2 family. After activation, it is able to form a heterodimer with anti-apoptotic proteins and prevent them from stopping apoptosis.

Mechanism of action

Bax/Bak are believed to initiate apoptosis by forming a pore in the mitochondrial outer membrane that allows cytochrome c to escape into the cytoplasm and activate the pro-apoptotic caspase cascade. The anti-apoptotic Bcl-2 and Bcl-xL proteins inhibit cytochrome c release through the mitochondrial pore and also inhibit activation of the cytoplasmic caspase cascade by cytochrome c.

Dephosphorylated BAD forms a heterodimer with Bcl-2 and Bcl-xL, inactivating them and thus allowing Bax/Bak-triggered apoptosis. When BAD is phosphorylated by Akt/protein kinase B (triggered by PIP3), it forms the BAD-(14-3-3) protein heterodimer. This leaves Bcl-2 free to inhibit Bax-triggered apoptosis. BAD phosphorylation is thus anti-apoptotic, and BAD dephosphorylation (e.g., by Ca2+-stimulated Calcineurin) is pro-apoptotic. The latter may be involved in neural diseases such as schizophrenia.

Interactions

Overview of signal transduction pathways involved with apoptosis.

Bcl-2-associated death promoter has been shown to interact with:

See also

Further reading

External links


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