Explore
Validate
Learn
Western blotAntibody data
- Antibody Data
- Antigen structure
- References [8]
- Comments [0]
- Validations [0]
Submit
Validation data
Reference
Comment
Report error
- Product number
- GTX14515 - Provider product page
- Provider
- GeneTex
- Proper citation
- GeneTex Cat#GTX14515, RRID:AB_845475
- Product name
- COMP antibody
- Antibody type
- Polyclonal
- Reactivity
- Human, Mouse, Rat
- Host
- Rabbit
Submitted references Mild myopathy is associated with COMP but not MATN3 mutations in mouse models of genetic skeletal diseases.
A novel transgenic mouse model of growth plate dysplasia reveals that decreased chondrocyte proliferation due to chronic ER stress is a key factor in reduced bone growth.
Armet/Manf and Creld2 are components of a specialized ER stress response provoked by inappropriate formation of disulphide bonds: implications for genetic skeletal diseases.
Analysis of the cartilage proteome from three different mouse models of genetic skeletal diseases reveals common and discrete disease signatures.
Loss of matrilin 1 does not exacerbate the skeletal phenotype in a mouse model of multiple epiphyseal dysplasia caused by a Matn3 V194D mutation.
A novel form of chondrocyte stress is triggered by a COMP mutation causing pseudoachondroplasia.
RB1CC1 protein suppresses type II collagen synthesis in chondrocytes and causes dwarfism.
A mouse model offers novel insights into the myopathy and tendinopathy often associated with pseudoachondroplasia and multiple epiphyseal dysplasia.
Piróg KA, Katakura Y, Mironov A, Briggs MD
PloS one 2013;8(11):e82412
PloS one 2013;8(11):e82412
A novel transgenic mouse model of growth plate dysplasia reveals that decreased chondrocyte proliferation due to chronic ER stress is a key factor in reduced bone growth.
Gualeni B, Rajpar MH, Kellogg A, Bell PA, Arvan P, Boot-Handford RP, Briggs MD
Disease models & mechanisms 2013 Nov;6(6):1414-25
Disease models & mechanisms 2013 Nov;6(6):1414-25
Armet/Manf and Creld2 are components of a specialized ER stress response provoked by inappropriate formation of disulphide bonds: implications for genetic skeletal diseases.
Hartley CL, Edwards S, Mullan L, Bell PA, Fresquet M, Boot-Handford RP, Briggs MD
Human molecular genetics 2013 Dec 20;22(25):5262-75
Human molecular genetics 2013 Dec 20;22(25):5262-75
Analysis of the cartilage proteome from three different mouse models of genetic skeletal diseases reveals common and discrete disease signatures.
Bell PA, Wagener R, Zaucke F, Koch M, Selley J, Warwood S, Knight D, Boot-Handford RP, Thornton DJ, Briggs MD
Biology open 2013 Aug 15;2(8):802-11
Biology open 2013 Aug 15;2(8):802-11
Loss of matrilin 1 does not exacerbate the skeletal phenotype in a mouse model of multiple epiphyseal dysplasia caused by a Matn3 V194D mutation.
Bell PA, Piróg KA, Fresquet M, Thornton DJ, Boot-Handford RP, Briggs MD
Arthritis and rheumatism 2012 May;64(5):1529-39
Arthritis and rheumatism 2012 May;64(5):1529-39
A novel form of chondrocyte stress is triggered by a COMP mutation causing pseudoachondroplasia.
Suleman F, Gualeni B, Gregson HJ, Leighton MP, Piróg KA, Edwards S, Holden P, Boot-Handford RP, Briggs MD
Human mutation 2012 Jan;33(1):218-31
Human mutation 2012 Jan;33(1):218-31
RB1CC1 protein suppresses type II collagen synthesis in chondrocytes and causes dwarfism.
Nishimura I, Chano T, Kita H, Matsusue Y, Okabe H
The Journal of biological chemistry 2011 Dec 23;286(51):43925-43932
The Journal of biological chemistry 2011 Dec 23;286(51):43925-43932
A mouse model offers novel insights into the myopathy and tendinopathy often associated with pseudoachondroplasia and multiple epiphyseal dysplasia.
Piróg KA, Jaka O, Katakura Y, Meadows RS, Kadler KE, Boot-Handford RP, Briggs MD
Human molecular genetics 2010 Jan 1;19(1):52-64
Human molecular genetics 2010 Jan 1;19(1):52-64
No comments: Submit comment
No validations: Submit validation data