BCL2L11

Source: Wikipedia, the free encyclopedia.
BCL2L11
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
Ensembl
UniProt
RefSeq (mRNA)

NM_001284410
NM_001291016
NM_009754
NM_207680
NM_207681

RefSeq (protein)
Location (UCSC)Chr 2: 111.12 – 111.17 MbChr 2: 127.97 – 128 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Bcl-2-like protein 11, commonly called BIM (Bcl-2 Interacting Mediator of cell death), is a protein that in humans is encoded by the BCL2L11 gene.[5][6]

Function

The protein encoded by this gene belongs to the

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 (FoxO3a), 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.[7]

Regulation of Bim

Bim expression and activity are regulated at the transcriptional, translational and post-translational levels; coordinated expression and activity of Bim shape immune responses, and ensure tissue integrity. Cancer cells develop mechanisms that suppress Bim expression, which allows for tumor progression and metastasis.[8]

Interactions

BCL2L11 has been shown to

interact
with:

See also

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000153094Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000027381Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^
    PMID 9731710
    .
  6. ^ .
  7. ^ "Entrez Gene: BCL2L11 BCL2-like 11 (apoptosis facilitator)".
  8. PMID 26405162
    .
  9. ^ .
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Further reading

External links