Search results for BCL2A1

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Protein (1 results from a total of 1)

Identifier: R-HSA-9725307
Species: Homo sapiens
Compartment: cytosol
Primary external reference: UniProt: BCL2A1: Q16548

DNA Sequence (1 results from a total of 1)

Identifier: R-HSA-9725309
Species: Homo sapiens
Compartment: nucleoplasm
Primary external reference: ENSEMBL: ENSEMBL:ENSG00000140379

Reaction (5 results from a total of 5)

Identifier: R-HSA-9858571
Species: Homo sapiens
Compartment: nucleoplasm, cytosol
BCL2A1 is an antiapoptotic member of the BCL2 family. It is expressed at low levels in the primary melanocytes and expressed at a higher level in a number of melanoma cell lines. The BCL2A1 gene is amplified in 30% of melanomas, a genetic alteration that appears unique to this cancer type and is not seen in other cancers examined. BCL2A1 expression is essential for survival in BCL2A1-amplified melanomas, and depends in part on the binding of MITF to an E-box element in the promoter (Haq et al, 2013; Strub et al, 2011; reviewed in Hartman and Czyz, 2015).
Identifier: R-HSA-9725338
Species: Homo sapiens
Compartment: nucleoplasm, cytosol
BCL2A1 was identified as a transcriptional target of the oncogenic NPM-ALK fusion protein through ALK knockdown and inhibition studies. BCL2A1 is a BCL2 family member that encodes an anti-apoptotic protein that, along with BAX2, is preferentially expressed by ALK signaling. shRNA-mediated knockdown of BCL2A1 promotes apoptosis, highlighting a critical role for BCL2A1 in mediating cellular survival (Piva et al, 2006; reviewed in Hallberg and Palmer, 2013).
Identifier: R-HSA-9858559
Species: Homo sapiens
Compartment: nucleoplasm
BCL2A1 is a anti-apoptotic member of the BCL2 family that is specifically upregulated in melanomas compared to other examined cancer types, and is genomically amplified in 30% of melanomas (Haq et al, 2013). BCL2A1 is expressed at high levels in melanoma cell lines and at a lower level in melanocytes, and is essential for survival in MITF- and BCL2A1-amplified lines (Haq et al, 2013). Expression of BCL2A1 is driven in part by the binding of MITF-M to an E-box element in the promoter as assessed by ChIP and reporter gene assay, and mutation of the E-box abrogates MITF-dependent expression (Strub et al, 2011; Haq et al, 2013). Suppression of BCL2A1 expression in melanoma cell lines inhibits cell growth and reduces the tumorigenicity in mouse xenografts (Haq et al, 2013; reviewed Hartman and Czyz, 2015).
Identifier: R-HSA-9725357
Species: Homo sapiens
Compartment: nucleoplasm, cytosol
CEBPB is a transcription factor with roles in immune and inflammatory reponses that was identified as a target of NPM-ALK signaling downstream of STAT3 and MAPK1/3 (Piva et al, 2006; Quintanilla-Martinez et al, 2006; Anastasov et al, 2010). CEBPB expression is downregulated after treatment of cells with anti-NPM-ALK RNAi or shRNA. CEBPB expression downstream of NPM-ALK signaling promotes cellular survival, as its knockdown increases the proportion of cells undergoing apoptosis. In mouse models of NPM-ALK, CEBPB is required for entry into S phase and contributes to the transforming properties of the fusion protein. (Piva et al, 2006; Quintanilla-Martinez et al, 2006; Anastasov et al, 2010; reviewed in Hallberg and Palmer, 2013).
Identifier: R-HSA-9725342
Species: Homo sapiens
Compartment: cytosol, nucleoplasm
NPM-ALK is known to drive expression of AP1 transcription factor family members, and AP1 targets are differentially expressed in ALK+ ALCLs compared to ALK- (Staber et al, 2007; Turner et al, 2007; Levantaki et al, 2007; Schleussner et al, 2018; reviewed in Ducray et al, 2019; Hallberg and Palmer, 2013; Garces de los Fayos Alonso et al, 2018). JUNB gene expression is driven downstream of NPM-ALK activity in anaplastic large cell lymphoma in a manner that is dependent on NPM-ALK kinase activity. NPM-ALK-mediated signaling stimulates transcriptional upregulation of JUNB through the MAP kinase signaling cascade and promotes accumulation of the JUNB protein through the PI3K/AKT signaling pathway. Consistent with this, treatment of NPM-ALK-expressing cells with either a MEK or a p70S6K inhibitor decreases JUNB levels and impairs cellular proliferation (Piva et al, 2006; Staber et al, 2007). Expression of AP1 components such as JUNB, JUN and FRA2 contribute to apoptosis and proliferation in ALCL cells (Mathas et al, 2002; Staber et al, 2007; Pearson et al, 2011).
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