BCL2L11: Difference between revisions

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=== Regulation of Bim ===
=== 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. <ref>{{cite journal | pmid = 26405162 | doi=10.18632/oncotarget.5492 | volume=6 | title=Regulation of Bim in Health and Disease | pmc=4695108 | journal=Oncotarget | pages=23058–134 | author=Sionov RV, Vlahopoulos SA, Granot Z}}</ref>
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.<ref name="pmid26405162">{{cite journal |vauthors = Sionov RV, Vlahopoulos SA, Granot Z |title = Regulation of Bim in Health and Disease |journal = Oncotarget |volume = 6 |issue = 27 |pages = 23058–134 |year = 2015 |pmid = 26405162 |pmc = 4695108 |doi = 10.18632/oncotarget.5492 }}</ref>


== Interactions ==
== Interactions ==
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*{{cite journal  | vauthors=Ohi N, Tokunaga A, Tsunoda H |title=A novel adenovirus E1B19K-binding protein B5 inhibits apoptosis induced by Nip3 by forming a heterodimer through the C-terminal hydrophobic region |journal=Cell Death Differ. |volume=6 |issue= 4 |pages= 314–25 |year= 1999 |pmid= 10381623 |doi= 10.1038/sj.cdd.4400493 |display-authors=etal}}
*{{cite journal  | vauthors=Ohi N, Tokunaga A, Tsunoda H |title=A novel adenovirus E1B19K-binding protein B5 inhibits apoptosis induced by Nip3 by forming a heterodimer through the C-terminal hydrophobic region |journal=Cell Death Differ. |volume=6 |issue= 4 |pages= 314–25 |year= 1999 |pmid= 10381623 |doi= 10.1038/sj.cdd.4400493 |display-authors=etal}}
*{{cite journal  | vauthors=Bouillet P, Metcalf D, Huang DC |title=Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity |journal=Science |volume=286 |issue= 5445 |pages= 1735–8 |year= 1999 |pmid= 10576740 |doi=10.1126/science.286.5445.1735  |display-authors=etal}}
*{{cite journal  | vauthors=Bouillet P, Metcalf D, Huang DC |title=Proapoptotic Bcl-2 relative Bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity |journal=Science |volume=286 |issue= 5445 |pages= 1735–8 |year= 1999 |pmid= 10576740 |doi=10.1126/science.286.5445.1735  |display-authors=etal}}
*{{cite journal  | vauthors=Bae J, Leo CP, Hsu SY, Hsueh AJ |title=MCL-1S, a splicing variant of the antiapoptotic BCL-2 family member MCL-1, encodes a proapoptotic protein possessing only the BH3 domain |journal=J. Biol. Chem. |volume=275 |issue= 33 |pages= 25255–61 |year= 2000 |pmid= 10837489 |doi= 10.1074/jbc.M909826199 }}
*{{cite journal  | vauthors=Dijkers PF, Medema RH, Lammers JW |title=Expression of the pro-apoptotic Bcl-2 family member Bim is regulated by the forkhead transcription factor FKHR-L1 |journal=Curr. Biol. |volume=10 |issue= 19 |pages= 1201–4 |year= 2000 |pmid= 11050388 |doi=10.1016/S0960-9822(00)00728-4  |display-authors=etal}}
*{{cite journal  | vauthors=Dijkers PF, Medema RH, Lammers JW |title=Expression of the pro-apoptotic Bcl-2 family member Bim is regulated by the forkhead transcription factor FKHR-L1 |journal=Curr. Biol. |volume=10 |issue= 19 |pages= 1201–4 |year= 2000 |pmid= 11050388 |doi=10.1016/S0960-9822(00)00728-4  |display-authors=etal}}
*{{cite journal  | vauthors=Bouillet P, Zhang LC, Huang DC |title=Gene structure alternative splicing, and chromosomal localization of pro-apoptotic Bcl-2 relative Bim |journal=Mamm. Genome |volume=12 |issue= 2 |pages= 163–8 |year= 2001 |pmid= 11210187 |doi=10.1007/s003350010242  |display-authors=etal}}
*{{cite journal  | vauthors=Bouillet P, Zhang LC, Huang DC |title=Gene structure alternative splicing, and chromosomal localization of pro-apoptotic Bcl-2 relative Bim |journal=Mamm. Genome |volume=12 |issue= 2 |pages= 163–8 |year= 2001 |pmid= 11210187 |doi=10.1007/s003350010242  |display-authors=etal}}

Latest revision as of 14:26, 28 January 2018

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

n/a

n/a

RefSeq (protein)

n/a

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Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

Bcl-2-like protein 11, commonly called BIM, is a protein that in humans is encoded by the BCL2L11 gene.[1][2]

Function

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 (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.[3]

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.[4]

Interactions

BCL2L11 has been shown to interact with:

See also

References

  1. 1.0 1.1 1.2 1.3 1.4 Hsu SY, Lin P, Hsueh AJ (November 1998). "BOD (Bcl-2-related ovarian death gene) is an ovarian BH3 domain-containing proapoptotic Bcl-2 protein capable of dimerization with diverse antiapoptotic Bcl-2 members". Mol Endocrinol. 12 (9): 1432–40. doi:10.1210/mend.12.9.0166. PMID 9731710.
  2. 2.0 2.1 2.2 2.3 O'Connor L, Strasser A, O'Reilly LA, Hausmann G, Adams JM, Cory S, Huang DC (February 1998). "Bim: a novel member of the Bcl-2 family that promotes apoptosis". EMBO J. 17 (2): 384–95. doi:10.1093/emboj/17.2.384. PMC 1170389. PMID 9430630.
  3. "Entrez Gene: BCL2L11 BCL2-like 11 (apoptosis facilitator)".
  4. Sionov RV, Vlahopoulos SA, Granot Z (2015). "Regulation of Bim in Health and Disease". Oncotarget. 6 (27): 23058–134. doi:10.18632/oncotarget.5492. PMC 4695108. PMID 26405162.
  5. 5.0 5.1 5.2 Chen L, Willis SN, Wei A, Smith BJ, Fletcher JI, Hinds MG, Colman PM, Day CL, Adams JM, Huang DC (February 2005). "Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function". Mol. Cell. 17 (3): 393–403. doi:10.1016/j.molcel.2004.12.030. PMID 15694340.
  6. Whitfield J, Harada K, Bardelle C, Staddon JM (November 2003). "High-throughput methods to detect dimerization of Bcl-2 family proteins". Anal. Biochem. 322 (2): 170–8. doi:10.1016/j.ab.2003.07.014. PMID 14596824.
  7. Day CL, Puthalakath H, Skea G, Strasser A, Barsukov I, Lian LY, Huang DC, Hinds MG (February 2004). "Localization of dynein light chains 1 and 2 and their pro-apoptotic ligands". Biochem. J. 377 (Pt 3): 597–605. doi:10.1042/BJ20031251. PMC 1223895. PMID 14561217.
  8. Vadlamudi RK, Bagheri-Yarmand R, Yang Z, Balasenthil S, Nguyen D, Sahin AA, den Hollander P, Kumar R (June 2004). "Dynein light chain 1, a p21-activated kinase 1-interacting substrate, promotes cancerous phenotypes". Cancer Cell. 5 (6): 575–85. doi:10.1016/j.ccr.2004.05.022. PMID 15193260.
  9. Bae J, Leo CP, Hsu SY, Hsueh AJ (August 2000). "MCL-1S, a splicing variant of the antiapoptotic BCL-2 family member MCL-1, encodes a proapoptotic protein possessing only the BH3 domain". J. Biol. Chem. 275 (33): 25255–61. doi:10.1074/jbc.M909826199. PMID 10837489.

Further reading

External links