Product nameAnti-COL11A1 antibody
See all COL11A1 primary antibodies
DescriptionRabbit polyclonal to COL11A1
Tested applicationsSuitable for: IHC-Fr, ICC/IF, WB, ELISAmore details
Species reactivityReacts with: Mouse, Human
Synthetic peptide from an internal sequence of Human COL11A1.
- K562 cells.
Storage instructionsShipped at 4°C. Store at -20°C. Stable for 12 months at -20°C.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Constituents: PBS, 50% Glycerol, 0.87% Sodium chloride
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab64883 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-Fr||Use at an assay dependent concentration.|
|ICC/IF||1/50. (see Abreview)|
|WB||1/500 - 1/1000. Detects a band of approximately >170 kDa (predicted molecular weight: 181 kDa).|
FunctionMay play an important role in fibrillogenesis by controlling lateral growth of collagen II fibrils.
Tissue specificityCartilage, placenta and some tumor or virally transformed cell lines. Isoforms using exon IIA or IIB are found in the cartilage while isoforms using only exon IIB are found in the tendon.
Involvement in diseaseDefects in COL11A1 are the cause of Stickler syndrome type 2 (STL2) [MIM:604841]; also known as Stickler syndrome vitreous type 2. STL2 is an autosomal dominant form of Stickler syndrome, an inherited disorder that associates ocular signs with more or less complete forms of Pierre Robin sequence, bone disorders and sensorineural deafness. Ocular disorders may include juvenile cataract, myopia, strabismus, vitreoretinal or chorioretinal degeneration, retinal detachment, and chronic uveitis. Robin sequence includes an opening in the roof of the mouth (a cleft palate), a large tongue (macroglossia), and a small lower jaw (micrognathia). Bones are affected by slight platyspondylisis and large, often defective epiphyses. Juvenile joint laxity is followed by early signs of arthrosis. The degree of hearing loss varies among affected individuals and may become more severe over time. Syndrome expressivity is variable.
Defects in COL11A1 are the cause of Marshall syndrome (MARSHS) [MIM:154780]. It is an autosomal dominant disorder with ocular, orofacial, auditory and skeletal manifestations. It shares several features with Stickler syndrome, such as midfacial hypoplasia, high myopia, and sensorineural-hearing deficit.
Sequence similaritiesBelongs to the fibrillar collagen family.
Contains 1 fibrillar collagen NC1 domain.
Contains 1 TSP N-terminal (TSPN) domain.
modificationsProlines at the third position of the tripeptide repeating unit (G-X-Y) are hydroxylated in some or all of the chains.
Cellular localizationSecreted > extracellular space > extracellular matrix.
- Information by UniProt
- COBA1_HUMAN antibody
- COL11A1 antibody
- COLL6 antibody
All lanes : Anti-COL11A1 antibody (ab64883) at 1/500 dilution
Lane 1 : extracts from K562 cells (5-30µg total protein)
Lane 2 : extracts from K562 cells (5-30µg total protein) and 5-10µg of the immunising peptide.
Predicted band size: 181 kDa
Observed band size: 181 kDa
ab64883 staining of frozen human fetal heart tissue sections (IHC-Fr). Sections were fixed with paraformaldehyde and permeabilized by saponin. The primary antibody was diluted 1/200 and incubated with the sample for 1 hour 30 minutes at 37°C. An Alexa Fluor conjugated goat anti-rabbit antibody was used as the secondary.
This image is courtesy of an anonymous Abreview (April 2009)
Immunohistochemical analysis of frozen murine ovary tissue taken from post-natal day 23-29 wild-type (+/+) and ERß-null (-/-) mice.
COL11A1 was stained with ab64883, at 1/200 dilution.
This product has been referenced in:
- Zheng C et al. Suppressing UPR-dependent overactivation of FGFR3 signaling ameliorates SLC26A2-deficient chondrodysplasias. EBioMedicine 40:695-709 (2019). Read more (PubMed: 30685387) »
- Wang Y & Wu X SMOC1 silencing suppresses the angiotensin II-induced myocardial fibrosis of mouse myocardial fibroblasts via affecting the BMP2/Smad pathway. Oncol Lett 16:2903-2910 (2018). Read more (PubMed: 30127878) »