COL1A1 (E8F4L) XP® Rabbit mAb (BSA and Azide Free) #81375
- WB
- IHC
- IF
Supporting Data
| REACTIVITY | H M |
| SENSITIVITY | Endogenous |
| MW (kDa) | 220 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
Product Information
Product Usage Information
This product is the carrier free version of product #72026. All data were generated using the same antibody clone in the standard formulation which contains BSA and glycerol.
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 Phe1196 of human COL1A1 protein.
Background
Type 1 collagen is the most abundant collagen in many human tissues, including bone, skin, and tendons. It is a trimeric complex composed of two molecules of COL1A1 (alpha-1 type 1 collagen) and one molecule of COL1A2 (alpha-2 type 1 collagen) (1-3). The expression levels of COL1A1 are regulated by multiple mechanisms, including mRNA stability, translation, and post-translational modification (3-5). Overexpression of COL1A1 has been positively associated with tissue fibrosis disorders, including systemic sclerosis (6), while loss-of-function mutations in the COL1A1 gene are a major causative factor for osteogenesis imperfecta (brittle bone disease) (7). Notably, COL1A1 expression levels have also been associated with tumor development in gastric, lung, thyroid, and breast cancers. Research studies suggest that upregulation of COL1A1 can generate a modified extracellular matrix environment that promotes cancer cell survival, proliferation, metastasis, and invasion (8-11).
- Prockop, D.J. and Kivirikko, K.I. (1995) Annu Rev Biochem 64, 403-34.
- Chang, S.W. et al. (2012) Biophys J 102, 640-8.
- Zhang, Y. and Stefanovic, B. (2016) Int J Mol Sci 17, 419.
- Parsons, C.J. et al. (2011) J Biol Chem 286, 8609-19.
- Cai, L. et al. (2010) J Mol Biol 395, 309-26.
- Jimenez, S.A. and Saitta, B. (1999) Springer Semin Immunopathol 21, 397-414.
- Forlino, A. et al. (2011) Nat Rev Endocrinol 7, 540-57.
- Li, J. et al. (2016) World J Surg Oncol 14, 297.
- Oleksiewicz, U. et al. (2017) J Cancer Res Clin Oncol 143, 1133-41.
- Barcus, C.E. et al. (2017) Breast Cancer Res 19, 9.
- Jolly, L.A. et al. (2016) Cancer Res 76, 1804-13.
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