COL1A1 (E3I2I) Rabbit mAb (BSA and Azide Free) #41514
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | |
| MW (kDa) | |
| Source/Isotype | Rabbit IgG |
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.
BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.
BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.
Formulation
Supplied in 1X PBS (10 mM Na2HPO4, 3 mM KCl, 2 mM KH2PO4, and 140 mM NaCl (pH 7.8)). BSA and Azide Free.
Storage
Store at -20°C. This product will freeze at -20°C so it is recommended to aliquot into single-use vials to avoid multiple freeze/thaw cycles. A slight precipitate may be present and can be dissolved by gently vortexing. This will not interfere with antibody performance.
Specificity / Sensitivity
COL1A1 (E3I2I) Rabbit mAb (BSA and Azide Free) detects endogenous levels of COL1A1.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to a fragment 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).
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- Jimenez, S.A. and Saitta, B. (1999) Springer Semin Immunopathol 21, 397-414.
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- 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.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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