cIAP2 Antibody (YA7358)
(Synonyms: API2, MIHC, RNF49, BIRC3, Baculoviral IAP repeat-containing protein 3, Apoptosis inhibitor 2, Cellular inhibitor of apoptosis 2, IAP homolog C, Inhibitor of apoptosis protein 1, RING finger protein 49, RING-type E3 ubiquitin transferase BIRC3, TNFR2-TRAF-signaling complex protein 1, C-IAP2, hIAP-1, hIAP1)cIAP2 Antibody (YA7358) is a Rabbit-derived and non-conjugated IgG, Kappa monoclonal antibody, targeting to cIAP2.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IHC-P, ICC/IF, IP, ELISA
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Reactivity :
Human
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Formulation:
Supplied in PBS (pH7.4) containing 50% glycerol, 0.05% Proclin 300, 0.05%BSA
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Conjugation:
Non-conjugated
Applications
| Application |
IHC-P
IHC-P: Immunohistochemistry-Paraffin
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WB
WB: Western Blot
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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IP
IP: Immunoprecipitation
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|---|---|---|---|---|---|
| Dilution Ratio | 1:200-1:500 | 1:2000-1:10000 | 1:200-1:1000 | 1:5000-1:20000 | 1:50-1:200 |
Product Details
cIAP2 Antibody (YA7358) is a Rabbit-derived and non-conjugated IgG, Kappa monoclonal antibody, targeting to cIAP2.
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Host Rabbit
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Clonality Monoclonal,Recombinant
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Species ReactivityHuman
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Observed Molecular WeightObserved band size: 68 kDaNote: 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: 68 kDa
The exact sequence is proprietary to MCE.
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) containing 50% glycerol, 0.05% Proclin 300, 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
cIAP-2 (cellular inhibitor of apoptosis protein 2, encoded by BIRC3) is a member of the inhibitor of apoptosis protein (IAP) family that functions as a signaling regulator linking cell survival, inflammatory responses, and programmed cell death pathways[1][2]. Mechanistically, cIAP-2 acts as an E3 ubiquitin ligase within TNF receptor and pattern-recognition receptor signaling complexes, where it contributes to ubiquitination-dependent activation of NF-κB signaling and downstream transcriptional programs that support cellular adaptation to stress and immune stimulation[3][4]. Through cooperation with TRAF family proteins, cIAP-2 participates in the regulation of receptor-mediated signaling networks that control apoptosis, innate immunity, and inflammatory responses[3][5]. In disease settings, altered BIRC3 expression or mutation has been associated with hematologic malignancies and other cancers, highlighting the importance of cIAP-2 in tumor cell survival and therapy response[6][7]. Compared with the closely related isoform cIAP-1 (BIRC2), cIAP-2 displays distinct expression kinetics and regulatory patterns; cIAP-2 is strongly inducible by inflammatory cytokines through NF-κB-dependent mechanisms, whereas cIAP-1 is more constitutively expressed and is thought to support rapid signaling events[4]. This distinction suggests that cIAP-2 may contribute preferentially to sustained or later-phase signaling responses following inflammatory stimulation[4]. For experimental applications, cIAP-2 is widely investigated as a target of SMAC mimetics and other IAP-directed compounds that promote cIAP degradation or disrupt cIAP-associated signaling complexes, providing useful tools for studying NF-κB regulation, apoptosis sensitivity, and anticancer therapeutic mechanisms[2][8].
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Subcellular Localization
Cytoplasm,Nucleus
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Expression
Tissue_Specificity: Highly expressed in fetal lung, and kidney. In the adult, expression is mainly seen in lymphoid tissues, including spleen, thymus and peripheral blood lymphocytes -
Isoforms & Post-Translational Modification
Q13489: 604 amino acids, molecular weight 68372 Da.
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Subunit
Interacts with PRSS25; interaction inhibits apoptotic suppressor activity
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SwissProt ID
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Synonyms
API2, MIHC, RNF49, BIRC3, Baculoviral IAP repeat-containing protein 3, Apoptosis inhibitor 2, Cellular inhibitor of apoptosis 2, IAP homolog C, Inhibitor of apoptosis protein 1, RING finger protein 49, RING-type E3 ubiquitin transferase BIRC3, TNFR2-TRAF-signaling complex protein 1, C-IAP2, hIAP-1, hIAP1
Documentation
[1]. Bertrand MJ, et al. Cellular inhibitors of apoptosis cIAP1 and cIAP2 are required for innate immunity signaling by the pattern recognition receptors NOD1 and NOD2. Immunity. 2009 Jun 19;30(6):789-801. [Content Brief]
[2]. Rabezanahary H, et al. Live virus neutralizing antibodies against pre and post Omicron strains in food and retail workers in Québec, Canada. Heliyon. 2024 May 21;10(10):e31026. [Content Brief]
[3]. Li Y, et al. Structure of natural killer cell receptor KLRG1 bound to E-cadherin reveals basis for MHC-independent missing self recognition. Immunity. 2009 Jul 17;31(1):35-46. [Content Brief]
[4]. Thorne A, et al. Differential regulation of BIRC2 and BIRC3 expression by inflammatory cytokines and glucocorticoids in pulmonary epithelial cells. PLoS One. 2023 Jun 8;18(6):e0286783. [Content Brief]
[5]. Lee MJ, et al. Time to HIV rebound after infusion of long-acting broadly neutralising antibodies 3BNC117-LS and 10-1074-LS and analytical treatment interruption (the RIO trial): a double-blind, randomised, placebo-controlled trial. Lancet HIV. 2026 May 27:S2352-3018(26)00059-7. [Content Brief]
[6]. Frazzi R. BIRC3 and BIRC5: multi-faceted inhibitors in cancer. Cell Biosci. 2021 Jan 7;11(1):8. doi: 10.1186/s13578-020-00521-0. PMID: 33413657; PMCID: PMC7792207. et al. BIRC3 and BIRC5: multi-faceted inhibitors in cancer. Cell Biosci. 2021 Jan 7;11(1):8. [Content Brief]
[7]. Yamato A, et al. Oncogenic activity of BIRC2 and BIRC3 mutants independent of nuclear factor-κB-activating potential. Cancer Sci. 2015 Sep;106(9):1137-42. [Content Brief]
[8]. Cossu F, et al. Computational and Experimental Characterization of NF023, A Candidate Anticancer Compound Inhibiting cIAP2/TRAF2 Assembly. J Chem Inf Model. 2020 Oct 26;60(10):5036-5044. [Content Brief]