Product Pathways - Metabolism
C1QBP (D7H12) XP® Rabbit mAb #6502
|6502S||100 µl (10 western blots)||---||In Stock||---|
|6502P||40 µl (4 western blots)||---||In Stock||---|
|6502||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Mouse, Rat, Monkey||Endogenous||28||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IHC-P=Immunohistochemistry (Paraffin), IF-IC=Immunofluorescence (Immunocytochemistry), F=Flow Cytometry
Specificity / Sensitivity
C1QBP (D7H12) XP® Rabbit mAb recognizes endogenous levels of total C1QBP protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human C1QBP protein.
Western blot analysis of extracts from various cell lines using C1QBP (D7H12) XP® Rabbit mAb.
Immunohistochemical analysis of paraffin-embedded human breast carcinoma using C1QBP (D7H12) XP® Rabbit mAb.
Immunohistochemical analysis of paraffin-embedded mouse ovary using C1QBP (D7H12) XP® Rabbit mAb.
Flow cytometric analysis of Hela cells using C1QBP (D7H12) XP® Rabbit mAb (blue) compared to concentration-matched Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (red). Anti-rabbit IgG (H+L), F(ab')2 Fragment (Alexa Fluor® 488 Conjugate) #4412 was used as a secondary antibody.
C1QBP, also referred to as p32, p33, gC1q receptor (gC1qR), and hyaluronic acid binding protein 1 (HABP1), was originally identified via its binding interactions with Splicing Factor (SF-2) (1). Multiple, diverse binding partners of C1QBP were subsequently identified, including the globular heads of complement component C1q, hyaluronic acid, selected protein kinases (2), the tumor suppressor ARF (3-5), and multiple antigens of bacterial and viral origin (6). Research studies have shown that C1QBP is overexpressed in a number of cancer cell types (7), and has been implicated in the Warburg effect, whereby cancer cells shift their metabolism from oxidative phosphorylation to glycolysis (7). C1QBP has also been shown to inhibit the Mitochondrial Permeability Transition (MPT) pore, possibly serving a protective function against damage from oxidative stress (8).
- Krainer, A.R. et al. (1991) Cell 66, 383-94.
- Storz, P. et al. (2000) J Biol Chem 275, 24601-7.
- Itahana, K. and Zhang, Y. (2008) Cancer Cell 13, 542-53.
- Reef, S. et al. (2007) Oncogene 26, 6677-83.
- Reef, S. et al. (2006) Mol Cell 22, 463-75.
- Peerschke, E.I. and Ghebrehiwet, B. (2007) Immunobiology 212, 333-42.
- Fogal, V. et al. (2010) Mol Cell Biol 30, 1303-18.
- McGee, A.M. and Baines, C.P. (2010) Biochem J 433, 119-25.
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For Research Use Only. Not For Use In Diagnostic Procedures.
XP® is a trademark of Cell Signaling Technology, Inc.
DRAQ5® is a registered trademark of Biostatus Limited.
Alexa Fluor® is a registered trademark of Molecular Probes, Inc.
Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.