Bim Antibody (YA10104)
(Synonyms: BIM, BCL2L11, Bcl-2-like protein 11, Bcl2-L-11, Bcl2-interacting mediator of cell death)Bim Antibody (YA10104) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Bim.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IHC-P
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in PBS(pH7.4), 50% glycerol, 0.05% Proclin300, 0.05%BSA
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Conjugation:
Non-conjugated
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Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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|---|---|---|
| Dilution Ratio | 1:1000-1:2000 | 1:100-1:500 |
Product Details
Bim Antibody (YA10104) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Bim.
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Host Rabbit
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Clonality Recombinant,Monoclonal
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 25 kDa
Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 22 kDa
Entrez Gene: 10018 Human ; 12125 Mouse ;
SwissProt: O43521 Human ; O54918 Mouse ;
OMIM: 603827 Human
Recombinant protein of Human Bim.
Endogenous
Protein A affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS(pH7.4), 50% glycerol, 0.05% Proclin300, 0.05%BSA
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Background
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Function
Bim (BCL2L11) is a critical BH3-only protein that functions as a master regulator of intrinsic apoptosis, playing essential roles in immune homeostasis, tumor suppression, and disease pathogenesis. Alternative splicing generates three major isoforms—BimEL, BimL, and BimS—each with distinct biological activities. BimEL is predominantly involved in transcriptional regulation and cellular stress responses, while BimL plays a unique role in lysosomal acidification and autophagy progression by acting as an adaptor for dynein-mediated lysosome positioning; loss of BimL impairs autophagic degradation, leading to p62 accumulation and defective autolysosome formation[1]. In contrast, BimS and BimAD are potent activators of Bax, directly triggering mitochondrial outer membrane permeabilization and caspase activation without requiring anti-apoptotic Bcl-2 family members[6]. Structurally, Bim exists as an intrinsically unstructured protein (IUP)， adopting a 'bead on a string' conformation where only the BH3 domain becomes ordered upon binding to pro-survival Bcl-2 proteins, enabling flexible interaction with multiple targets[2]. Notably, Bim exhibits a double-bolt locking mechanism by simultaneously binding both Bcl-XL and Bcl-2 via its canonical BH3 domain and a C-terminal region (residues 181-192)， rendering it highly resistant to displacement by current BH3-mimetic drugs, which has significant implications for cancer therapy resistance[5]. In physiological contexts, Bim is indispensable for shaping adaptive immune responses: its absence leads to autoimmunity, while premature induction causes chronic inflammation and tumor progression[3]. Conversely, excessive Bim expression contributes to neurodegenerative disorders such as Alzheimer’s, Parkinson’s, and Huntington’s diseases, and is implicated in type I diabetes through β-cell apoptosis[3]. In cancer, Bim acts as a tumor suppressor; its downregulation or functional inactivation—via mechanisms including deletion polymorphisms in the BIM gene, proteasomal degradation (e.g., via Cul5Wsb2)， or viral hijacking (e.g., ASFV CD2v-induced ERK signaling) —promotes survival and therapeutic resistance[4,7,8,10]. Therapeutic strategies targeting Bim include HDAC inhibitors like SB939, which correct aberrant splicing in CML patients with BIM deletion polymorphisms, restoring TKI sensitivity[9], and splice-switching antisense oligonucleotides that rescue pro-apoptotic isoform expression[10]. These findings underscore Bim as a central node in cell death regulation and a promising target for precision medicine in oncology and degenerative diseases.
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Subcellular Localization
Endomembrane system; Peripheral membrane protein; Mitochondrion; Mitochondrion; Mitochondrion; Mitochondrion
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Expression
Tissue_specificity:The three main subtypes, BimEL, BimL, and BimS, are widely expressed, but exhibit tissue-specific differences. The Bim-γ subtype is most abundantly expressed in the small intestine and colon, with lower expression levels in the spleen, prostate, testis, heart, liver, and kidney.
Induction:By ER stress in a DDIT3/CHOP-dependent manner -
Isoforms & Post-Translational Modification
O43521 has 20 isomers: O43521-1: 22171 Da (predicted); O43521-2: 15967 Da (predicted); O43521-3: 12717 Da (predicted); O43521-4: 18536 Da (predicted); O43521-5: 12332 Da (predicted); O43521-6: 9081 Da (predicted); O43521-7: 9596 Da (predicted); O43521-8: 18816 Da (predicted); O43521-9: 9362 Da (predicted); O43521-10: 14458 Da (predicted); O43521-11: 14418 Da (predicted); O43521-12: 22649 Da (predicted); O43521-13: 4834 Da (predicted); O43521-14: 15025 Da (predicted); O43521-15: 8214 Da (predicted); O43521-16: 8821 Da (predicted); O43521-17: 12412 Da (predicted); O43521-18: 11773 Da (predicted); O43521-19: 17977 Da (predicted); O43521-20: 8523 Da (predicted).
Phosphorylation at Ser-69 by MAPK1/MAPK3 leads to interaction with TRIM2 and polyubiquitination, followed by proteasomal degradation (PubMed:15486195, PubMed:21478148). 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 -
Subunit
Forms heterodimers with a number of antiapoptotic Bcl-2 proteins, including MCL1, BCL2, BCL2L1 isoform Bcl-X(L), BCL2A1/BFL-1, BHRF1, and BCL2L2/BCLW (PubMed:11997495, PubMed:18812174, PubMed:27013495). Does not heterodimerize with proapoptotic proteins such as BAD, BOK or BAK. Identified in a complex containing BCL2L11, DYNLL1 and BCL2L1 isoform Bcl-X(L); BH3 integrity is required for BCL2L1-binding. Interacts with YWHAZ. When phosphorylated, interacts with TRIM2; this interaction is associated with ubiquitination and degradation (PubMed:21478148). Interacts with MCL1; may sequester BCL2L11 to prevent its pro-apoptotic activity (PubMed:17389404, PubMed:27013495). Interacts with GIMAP5 (PubMed:16509771). Interacts with BCL2L10/BCL-B (PubMed:22498477, PubMed:23235460, PubMed:23563182)
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SwissProt ID
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Synonyms
BIM, BCL2L11, Bcl-2-like protein 11, Bcl2-L-11, Bcl2-interacting mediator of cell death
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Research Field
Cell Biology
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