Lane 1: Raji cell lysate
Lane 2: Jurkat cell lysate
Lane 3: A431 cell lysate
Recombinant Rabbit monoclonal primary
Recombinant Bim Monoclonal Antibody (ET1608-14)
Raji cell lysate, Jurkat cell lysate, A431 cell lysate, Hela, A431, HepG2, human breast carcinoma tissue.
Store at +4C after thawing. Aliquot store at -20C or -80C. Avoid repeated freeze / thaw cycles.
1*TBS (pH7.4), 0.05% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.
Protein A affinity purified.
BCL2 like 11 antibody; B2L11_HUMAN antibody; BAM antibody; Bcl 2 interacting protein Bim antibody; Bcl 2 related ovarian death agonist antibody; Bcl-2-like protein 11 antibody; BCL2 interacting mediator of cell death antibody; BCL2 like 11 (apoptosis facilitator) antibody; BCL2 like protein 11 antibody; Bcl2-interacting mediator of cell death antibody; Bcl2-L-11 antibody; Bcl2l11 antibody; BIM alpha6 antibody; BIM antibody; BIM beta6 antibody; BIM beta7 antibody; BimEL antibody; BimL antibody; BOD antibody
Belongs to the Bcl-2 family.
Isoform BimEL, isoform BimL and isoform BimS are the predominant isoforms and are widely expressed with tissue-specific variation. Isoform Bim-gamma is most abundantly expressed in small intestine and colon, and in lower levels in spleen, prostate, testis, heart, liver and kidney.
Phosphorylation at Ser-69 by MAPK1/MAPK3 leads to interaction with TRIM2 and polyubiquitination, followed by proteasomal degradation. Deubiquitination catalyzed by USP27X stabilizes the protein (By similarity).; Ubiquitination by TRIM2 following phosphorylation by MAPK1/MAPK3 leads to proteasomal degradation. Conversely, deubiquitination catalyzed by USP27X stabilizes the protein.
Endomembrane system, Mitochondrion.
Pro-apototic Bcl-2 family members promote cell death by neutralizing their anti-apoptotic relatives, which otherwise maintain cell viability by regulating caspase activity. Bim belongs to the BH3-only subgroup of Bcl-2 related proteins, and exists in three distinct isoforms, BimS (short), BimL (long) and BimEL (extra long). ERK1/2 phosphorylates BimEL, resulting in rapid degradation of the isoform via the proteasome pathway. At least three sites for ERK1/2 phosphorylation exist on BimEL, whereas ERK1/2 does not effect BimS and BimL, implying a unique role for BimEL in cell survival signaling.