Product nameAnti-Collagen I antibody
See all Collagen I primary antibodies
DescriptionRabbit polyclonal to Collagen I
Tested applicationsSuitable for: IHC-Fr, RIA, ELISA, WB, ICC/IF, IHC-Pmore details
Species reactivityReacts with: Mouse
Collagen type I extracted and purified from mouse skin.
- Frozen mouse liver for IF.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Concentration information loading...
Purification notesPurified by Ion exchange chromatography (DEAE-Trisacryl).
- Human Collagen I peptide (ab101220)
- Prestained Protein Ladder - Broad molecular weight (10-245 kDa) (ab116028)
- Mouse Pro-Collagen I alpha 1 ELISA Kit (ab210579)
- Mouse Pro-Collagen I alpha 1 Matched Antibody Pair Kit (ab216791)
- Native Cow Collagen I protein (ab7526)
- Native Human Collagen I protein (ab7533)
Our Abpromise guarantee covers the use of ab21286 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-Fr||1/40. Tested using a FITC-labeled anti-rabbit IgG secondary.|
|ELISA||Use at an assay dependent concentration.|
|WB||Use at an assay dependent concentration.|
|ICC/IF||Use at an assay dependent concentration.|
|IHC-P||1/250. Tested using an HRP-labeled anti-rabbit IgG secondary.|
FunctionType I collagen is a member of group I collagen (fibrillar forming collagen).
Tissue specificityForms the fibrils of tendon, ligaments and bones. In bones the fibrils are mineralized with calcium hydroxyapatite.
Involvement in diseaseDefects in COL1A1 are the cause of Caffey disease (CAFFD) [MIM:114000]; also known as infantile cortical hyperostosis. Caffey disease is characterized by an infantile episode of massive subperiosteal new bone formation that typically involves the diaphyses of the long bones, mandible, and clavicles. The involved bones may also appear inflamed, with painful swelling and systemic fever often accompanying the illness. The bone changes usually begin before 5 months of age and resolve before 2 years of age.
Defects in COL1A1 are a cause of Ehlers-Danlos syndrome type 1 (EDS1) [MIM:130000]; also known as Ehlers-Danlos syndrome gravis. EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS1 is the severe form of classic Ehlers-Danlos syndrome.
Defects in COL1A1 are the cause of Ehlers-Danlos syndrome type 7A (EDS7A) [MIM:130060]; also known as autosomal dominant Ehlers-Danlos syndrome type VII. EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS7A is marked by bilateral congenital hip dislocation, hyperlaxity of the joints, and recurrent partial dislocations.
Defects in COL1A1 are a cause of osteogenesis imperfecta type 1 (OI1) [MIM:166200]. A dominantly inherited connective tissue disorder characterized by bone fragility and blue sclerae. Osteogenesis imperfecta type 1 is non-deforming with normal height or mild short stature, and no dentinogenesis imperfecta.
Defects in COL1A1 are a cause of osteogenesis imperfecta type 2A (OI2A) [MIM:166210]; also known as osteogenesis imperfecta congenita. A connective tissue disorder characterized by bone fragility, with many perinatal fractures, severe bowing of long bones, undermineralization, and death in the perinatal period due to respiratory insufficiency.
Defects in COL1A1 are a cause of osteogenesis imperfecta type 3 (OI3) [MIM:259420]. A connective tissue disorder characterized by progressively deforming bones, very short stature, a triangular face, severe scoliosis, grayish sclera, and dentinogenesis imperfecta.
Defects in COL1A1 are a cause of osteogenesis imperfecta type 4 (OI4) [MIM:166220]; also known as osteogenesis imperfecta with normal sclerae. A connective tissue disorder characterized by moderately short stature, mild to moderate scoliosis, grayish or white sclera and dentinogenesis imperfecta.
Genetic variations in COL1A1 are a cause of susceptibility to osteoporosis (OSTEOP) [MIM:166710]; also known as involutional or senile osteoporosis or postmenopausal osteoporosis. Osteoporosis is characterized by reduced bone mass, disruption of bone microarchitecture without alteration in the composition of bone. Osteoporotic bones are more at risk of fracture.
Note=A chromosomal aberration involving COL1A1 is found in dermatofibrosarcoma protuberans. Translocation t(17;22)(q22;q13) with PDGF.
Sequence similaritiesBelongs to the fibrillar collagen family.
Contains 1 fibrillar collagen NC1 domain.
Contains 1 VWFC domain.
modificationsProline residues at the third position of the tripeptide repeating unit (G-X-Y) are hydroxylated in some or all of the chains. Proline residues at the second position of the tripeptide repeating unit (G-X-Y) are hydroxylated in some of the chains.
O-linked glycan consists of a Glc-Gal disaccharide bound to the oxygen atom of a post-translationally added hydroxyl group.
Cellular localizationSecreted > extracellular space > extracellular matrix.
- Information by UniProt
- Alpha 1 type I collagen antibody
- Alpha 2 type I collagen antibody
- alpha 2 type I procollagen antibody
ab21286 staining collagen 1 in Mouse small intestine tissue sections by Immunohistochemistry (IHC-P - paraformaldehyde-fixed, paraffin-embedded sections). Tissue was fixed with paraformaldehyde and blocked with 10% serum for 20 minutes at 23°C; antigen retrieval was by heat mediation. Samples were incubated with primary antibody (1/250 in TBS (1% Tween) + 10% Goat Serum) for 24 hours at 4°C. A goat anti-rabbit Alexa Fluor®488 (ab150077) polyclonal was used as the secondary antibody.
ab21286 staining Collagen I (red) in Mouse colon tumor cells by ICC/IF (Immunocytochemistry/immunofluorescence). Cells were fixed with paraformaldehyde, permeabilized boiling in citrate buffer and blocked with 1% BSA for 30 minutes at 25°C. Samples were incubated with primary antibody (1/250 in PBS + 1% BSA) for 12 hours at 4°C. ab96897, goat anti-rabbit DyLight®594 (1/1000) was used as the secondary antibody. Costained with Rabbit anti-E Cadherin (green).
Anti-Collagen I antibody (ab21286) at 1/250 dilution + Mouse tail tendon collagen at 4 µg
goat anti-rabbit IgG-IRDye 800 conjugated at 1/2500 dilution
Performed under non-reducing conditions.
Observed band size: 115,120 kDa why is the actual band size different from the predicted?
Exposure time: 3 minutes
ab21286 staining Collagen I in Mouse intestinal adenoma tissue sections by Immunohistochemistry (IHC-P - paraformaldehyde-fixed, paraffin-embedded sections). Tissue was fixed with 10% NBF; antigen retrieval was by heat mediation in a citrate buffer. Samples were incubated with primary antibody (1/200 in PBS) for 16 hours at 4°C. A Biotin-conjugated Goat anti-rabbit polyclonal (1/250) was used as the secondary antibody.
ab21286 at a 1/200 dilution staining Collagen I in mouse parietal tissue by Immunohistochemistry (PFA fixed, frozen sections), incubated for 16 hours at 4°C. Permeabilized with 0.1% Triton. Blocked using 20% serum for 1 hour at room temperature. Secondary used polyclonal donkey conjugated to Alexa Fluor 555 (green).
ab21286 at 1/200 staining mouse embryonic lung tissue by IHC-P. The tissue was paraformaldehyde fixed and blocked with serum. A heat mediated antigen retrieval step was performed and the tissue was then stained with the antibody for 15 hours. A biotinylated goat anti-rabbit IgG antibody was used as the secondary.
This product has been referenced in:
- Jiang B et al. The inhibition of glycosaminoglycan incorporation influences the cell proliferation and cytodifferentiation in cultured embryonic mouse molars. J Mol Histol 50:11-19 (2019). Read more (PubMed: 30498999) »
- Zhang S et al. Osthole Ameliorates Renal Fibrosis in Mice by Suppressing Fibroblast Activation and Epithelial-Mesenchymal Transition. Front Physiol 9:1650 (2018). Read more (PubMed: 30524310) »