HMGA1 (D4F8) Rabbit mAb #12094
- WB
- IHC
- IF
Supporting Data
REACTIVITY | H Mk |
SENSITIVITY | Endogenous |
MW (kDa) | 18 |
Source/Isotype | Rabbit |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
- Mk-Monkey
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Immunohistochemistry (Paraffin) | 1:2000 |
Immunofluorescence (Immunocytochemistry) | 1:200 |
Storage
Protocol
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.
Species Reactivity:
Human, Monkey
The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.
Species predicted to react based on 100% sequence homology:
Bovine
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly68 of human HMGA1 protein.
Background
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).
Limited Uses
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