CA9 (D10C10) Rabbit mAb (BSA and Azide Free) #83980
- WB
- IHC
Supporting Data
REACTIVITY | H |
SENSITIVITY | Endogenous |
MW (kDa) | 35-58 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
Formulation
Storage
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asp361 of human CA9 protein.
Background
Carbonic anhydrases (CA) are a family of ancient zinc metalloenzymes found in almost all living organisms. All CA can be divided into 3 distinct classes (α, β, and γ) that evolved independently and have no significant homology in sequence and overall folding. All functional CA catalyze the reversible hydration of CO2 into HCO3- and H+ and contain a zinc atom in the active sites essential for catalysis. There are many isoforms of CA in mammals and they all belong to the α class (1,2).
CA9 is a member of alpha class, a plasma membrane protein with the catalytic domain in the extracellular space. Its expression is restricted to very few normal tissues (mainly the gastrointestinal tract) (2). CA9 expression is strongly induced by hypoxia and down-regulated by the wildtype von Hippel–Lindau (VHL) tumor suppressor protein. CA9 expression is increased in many types of tumor, especially in solid hypoxic tumors with a poor responsiveness to the conventional radio-and/or chemo-therapies; CA9 is considered as a tumor hypoxia marker and a promising target for cancer therapeutic intervention (3-5).
- Smith, K.S. et al. (1999) Proc Natl Acad Sci USA 96, 15184-9.
- Tripp, B.C. et al. (2001) J Biol Chem 276, 48615-8.
- Potter, C.P. and Harris, A.L. (2003) Br J Cancer 89, 2-7.
- Winum, J.Y. et al. (2009) Anticancer Agents Med Chem 9, 693-702.
- De Simone, G. and Supuran, C.T. (2010) Biochim Biophys Acta 1804, 404-9.
Limited Uses
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