Product Pathways - Chromatin Regulation / Epigenetics
HMGA1 (D4F8) Rabbit mAb #12094
|12094S||100 µl (10 western blots)||---||In Stock||---|
|12094||carrier free and custom formulation / quantity||email request|
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Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IHC-P=Immunohistochemistry (Paraffin), IF-IC=Immunofluorescence (Immunocytochemistry)
Species predicted to react based on 100% sequence homology: Bovine.
Specificity / Sensitivity
HMGA1 (D4F8) Rabbit mAb recognizes endogenous levels of total HMGA1 protein, isoforms 1a and 1b. Based on sequence homology, this antibody is not predicted to cross-react with HMGA2.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly68 of human HMGA1 protein.
Western blot analysis of extracts from NCCIT and NTERA2 cl.D1 cells using HMGA1 (D4F8) Rabbit mAb.
Immunohistochemical analysis of paraffin-embedded human lung carcinoma using HMGA1 (D4F8) Rabbit mAb.
Immunohistochemical analysis of paraffin-embedded human colon carcinoma using HMGA1 (D4F8) Rabbit mAb in the presence of control peptide (left) or antigen-specific peptide (right).
HMGA1, formerly known as HMG-I/Y, belongs to a family of high mobility group proteins that contain an AT-hook DNA binding domain. HMGA proteins are considered architectural transcription factors; they do not have direct transcriptional activation capacity, but instead regulate gene expression by changing DNA conformation through binding to AT-rich regions in the DNA and/or direct interaction with other transcription factors (1,2). HMGA1 is highly expressed during embryogenesis and in embryonic stem cells, but not in fully differentiated adult tissues (2-4). Research studies have shown that HMGA1 is over-expressed in rapidly dividing neoplastic cells and a wide variety of aggressive cancers, including thyroid, colon, breast, pancreas, and prostate (2-4). Investigators have shown that forced expression of HMGA1 induces cellular transformation and an epithelial-to-mesenchymal transition (EMT), while inhibition of HMGA1 expression blocks anchorage-independent cell growth and proliferation of cancer cells, suggesting that HMGA1 contributes to carcinogenesis by inducing and maintaining a de-differentiated, highly proliferative cell state (5-8).
- Cleynen, I. and Van de Ven, W.J. (2008) Int J Oncol 32, 289-305.
- Resar, L.M. (2010) Cancer Res 70, 436-9.
- Chiappetta, G. et al. (1996) Oncogene 13, 2439-46.
- Ben-Porath, I. et al. (2008) Nat Genet 40, 499-507.
- Wood, L.J. et al. (2000) Mol Cell Biol 20, 5490-502.
- Wood, L.J. et al. (2000) Cancer Res 60, 4256-61.
- Xu, Y. et al. (2004) Cancer Res 64, 3371-5.
- Scala, S. et al. (2000) Proc Natl Acad Sci U S A 97, 4256-61.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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