Anti-Caspase 10 antibody (ab27525)
- Product nameAnti-Caspase 10 antibodySee all Caspase 10 primary antibodies ...
- DescriptionRabbit polyclonal to Caspase 10
- Specificityab27525 recognises CASPASE 10.
- Tested applicationsIHC-P more details
- Species reactivityReacts with: Human
Synthetic peptide (Human)(N terminal)
- Positive controlNIH/3T3. Lung carcinoma
- Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
- Storage bufferPreservative: 0.1% Sodium Azide
Constituents: 1% BSA, 10mM PBS, pH 7.4
- Concentration information loading...
- PurityProtein A purified
- Clonality Polyclonal
- Research Areas
Our Abpromise guarantee covers the use of ab27525 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Not yet tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
- FunctionInvolved in the activation cascade of caspases responsible for apoptosis execution. Recruited to both Fas- and TNFR-1 receptors in a FADD dependent manner. May participate in the granzyme B apoptotic pathways. Cleaves and activates caspase-3, -4, -6, -7, -8, and -9. Hydrolyzes the small- molecule substrates, Tyr-Val-Ala-Asp-
-AMC and Asp-Glu-Val-Asp-
Isoform C is proteolytically inactive.
- Tissue specificityDetectable in most tissues. Lowest expression is seen in brain, kidney, prostate, testis and colon.
- Involvement in diseaseDefects in CASP10 are the cause of autoimmune lymphoproliferative syndrome type 2A (ALPS2A) [MIM:603909]. ALPS2 is characterized by abnormal lymphocyte and dendritic cell homeostasis and immune regulatory defects.
Defects in CASP10 are a cause of familial non-Hodgkin lymphoma (NHL) [MIM:605027]. NHL is a cancer that starts in cells of the lymph system, which is part of the body's immune system. NHLs can occur at any age and are often marked by enlarged lymph nodes, fever and weight loss.
Defects in CASP10 are a cause of gastric cancer (GASC) [MIM:613659]. A malignant disease which starts in the stomach, can spread to the esophagus or the small intestine, and can extend through the stomach wall to nearby lymph nodes and organs. It also can metastasize to other parts of the body. The term gastric cancer or gastric carcinoma refers to adenocarcinoma of the stomach that accounts for most of all gastric malignant tumors. Two main histologic types are recognized, diffuse type and intestinal type carcinomas. Diffuse tumors are poorly differentiated infiltrating lesions resulting in thickening of the stomach. In contrast, intestinal tumors are usually exophytic, often ulcerating, and associated with intestinal metaplasia of the stomach, most often observed in sporadic disease.
- Sequence similaritiesBelongs to the peptidase C14A family.
Contains 2 DED (death effector) domains.
modificationsCleavage by granzyme B and autocatalytic activity generate the two active subunits.
Phosphorylated upon DNA damage, probably by ATM or ATR.
- ALPS 2 antibodyALPS2 antibodyApoptosis related cysteine peptidase antibody
- Apoptotic protease Mch 4 antibodyApoptotic protease Mch-4 antibodyCASP 10 antibodyCASP-10 antibodyCASP10 antibodyCASP10 antibodyCASP10 protein antibodyCASPA_HUMAN antibodyCaspase 10 apoptosis related cysteine peptidase antibodyCaspase 10 apoptosis related cysteine protease antibodyCaspase-10 subunit p12 antibodyCaspase10 antibodyFADD Like Ice 2 antibodyFADD Like Ice 2 antibodyFADD like ICE2 antibodyFas Associated Death Domain Protein antibodyFAS associated death domain protein interleukin 1B converting enzyme 2 antibodyFAS-associated death domain protein interleukin-1B-converting enzyme 2 antibodyFLICE 2 antibodyFLICE2 antibodyFLICE2 antibodyICE Like Apoptotic Protease 4 antibodyICE-like apoptotic protease 4 antibodyInterleukin 1B Converting Enzyme 2 antibodyInterleukin 1B Converting Enzyme 2 antibodyMCH 4 antibodyMCH4 antibodyMCH4 antibody
References for Anti-Caspase 10 antibody (ab27525)
ab27525 has not yet been referenced specifically in any publications.