Caspase-10 Antibody (YA2366)
(Synonyms: CASP10; MCH4; Caspase-10; CASP-10; Apoptotic protease Mch-4; FAS-associated death domain protein interleukin-1B-converting enzyme 2; FLICE2; ICE-like apoptotic protease 4)Caspase-10 Antibody (YA2366) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Caspase-10.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IHC-P, IP
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Reactivity :
Human
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Formulation:
Supplied in 50mM Tris-Glycine(pH 7.4), 0.15M NaCl, 40% Glycerol, 0.01% Sodium azide and 0.05% BSA
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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IP
IP: Immunoprecipitation
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|---|---|---|---|
| Dilution Ratio | 1:500-1:1000 | 1:50-1:100 | 1:20 |
Product Details
Caspase-10 Antibody (YA2366) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Caspase-10.
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Host Rabbit
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Clonality Recombinant,Monoclonal
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Species ReactivityHuman
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Observed Molecular WeightObserved band size: 59 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: 59 kDa
Recombinant protein of human Caspase-10
Endogenous
Affinity Purified
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in 50mM Tris-Glycine(pH 7.4), 0.15M NaCl, 40% Glycerol, 0.01% Sodium azide and 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
Caspase-10 (CASP10) functions as an initiator caspase in death receptor signaling and can initiate Fas- and TRAIL-receptor-mediated apoptosis independently of caspase-8[1]. Mechanistically, caspase-10 is recruited to native TRAIL and CD95/Fas death-inducing signaling complexes (DISC) in a FADD-dependent manner, but it cannot functionally substitute caspase-8 in caspase-8-deficient cells[2]. Compared with caspase-8, caspase-10 acts as a regulatory isoform that reduces caspase-8 DISC association and activation, thereby switching CD95L signaling toward NF-κB activation and cell survival[3]. Caspase-8 and caspase-10 also activate NF-κB through RIP, NIK, and IKKα kinases, linking apoptotic machinery to inflammatory gene regulation[4]. In primary biliary cholangitis models, caspase-10 knockout macrophages showed stronger regulation of inflammatory cell death than caspase-8 knockout macrophages, including necroptosis and pyroptosis[5]. CASP10 mutations were reported in autoimmune lymphoproliferative syndrome type II with defective lymphocyte and dendritic cell apoptosis, but later human variant analyses found CASP10 dispensable for Fas-mediated apoptosis and unlikely to drive ALPS pathogenesis[6][7]. Substrate studies show overlapping caspase-8/caspase-10 cleavage preferences for RIP and PAK2, but distinct Bid cleavage patterns[8]. For experimental applications, the caspase-10 inhibitor z-AEVD-Fmk reduced terminal erythroid differentiation in CD36+ cultures, supporting pathway-specific functional testing[9].
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Expression
Tissue_specificity:It can be detected in most tissues. The lowest expression levels are found in the brain, kidneys, prostate, testes, and colon. -
Isoforms & Post-Translational Modification
Q92851 has 7 isomers: Q92851-1: 58951 Da (predicted); Q92851-2: 54566 Da (predicted); Q92851-4: 58994 Da (predicted); Q92851-3: 31419 Da (predicted); Q92851-5: 54523 Da (predicted); Q92851-6: 51785 Da (predicted); Q92851-7: 28364 Da (predicted).
Cleavage by granzyme B and autocatalytic activity generate the two active subunits -
Subunit
Heterotetramer that consists of two anti-parallel arranged heterodimers, each one formed by a 23/17 kDa (p23/17) (depending on the splicing events) and a 12 kDa (p12) subunit (By similarity). Self-associates. Interacts with FADD and CASP8. Found in a Fas signaling complex consisting of FAS, FADD, CASP8 and CASP10. Interacts with RFFL and RNF34; negatively regulate CASP10 through proteasomal degradation. Interacts with RIOK3
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SwissProt ID
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Synonyms
CASP10; MCH4; Caspase-10; CASP-10; Apoptotic protease Mch-4; FAS-associated death domain protein interleukin-1B-converting enzyme 2; FLICE2; ICE-like apoptotic protease 4
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Research Field
Cell Biology
Documentation
References
[1]. Wang J, et al. Caspase-10 is an initiator caspase in death receptor signaling. Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13884-8. [Content Brief]
[2]. Sprick MR, et al. Caspase-10 is recruited to and activated at the native TRAIL and CD95 death-inducing signalling complexes in a FADD-dependent manner but can not functionally substitute caspase-8. EMBO J. 2002 Sep 2;21(17):4520-30. [Content Brief]
[3]. Horn S, et al. Caspase-10 Negatively Regulates Caspase-8-Mediated Cell Death, Switching the Response to CD95L in Favor of NF-κB Activation and Cell Survival. Cell Rep. 2017 Apr 25;19(4):785-797. [Content Brief]
[4]. Shikama Y, et al. Caspase-8 and caspase-10 activate NF-kappaB through RIP, NIK and IKKalpha kinases. Eur J Immunol. 2003 Jul;33(7):1998-2006. [Content Brief]
[5]. Cho M, et al. Caspase-10 affects the pathogenesis of primary biliary cholangitis by regulating inflammatory cell death. J Autoimmun. 2022 Dec;133:102940. [Content Brief]
[6]. Wang J, et al. Inherited human Caspase 10 mutations underlie defective lymphocyte and dendritic cell apoptosis in autoimmune lymphoproliferative syndrome type II. Cell. 1999 Jul 9;98(1):47-58. [Content Brief]
[7]. Consonni F, et al. Study of the potential role of CASPASE-10 mutations in the development of autoimmune lymphoproliferative syndrome. Cell Death Dis. 2024 May 4;15(5):315. [Content Brief]
[8]. Fischer U, et al. Unique and overlapping substrate specificities of caspase-8 and caspase-10. Oncogene. 2006 Jan 5;25(1):152-9. [Content Brief]
[9]. Lamarque M, et al. Role of Caspase-10-P13tBID axis in erythropoiesis regulation. Cell Death Differ. 2023 Jan;30(1):208-220. [Content Brief]
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