Rabbit anti-Human MMP13 Polyclonal Antibody | anti-MMP13 antibody
MMP13, ID (MMP13, Collagenase 3, Matrix metalloproteinase-13) (Biotin)
Western Blot (WB)
(Western Blot analysis in K562 cell line lysates (35ug/lane) usingMBS647316. This demonstrates that MBS647316 detected the MMP13 protein (arrow).)
Immunohistochemistry (IHC)
(Immunohistochemistry analysis in formalin fixed and paraffin embedded human breast carcinoma using MBS647316 followed by peroxidase conjugation of the secondary antibody and DAB staining. This data demonstrates the use of MBS647316 for immunohistochemistry.)
NCBI and Uniprot Product Information
NCBI Description
Proteins of the matrix metalloproteinase (MMP) family are involved in the breakdown of extracellular matrix in normal physiological processes, such as embryonic development, reproduction, and tissue remodeling, as well as in disease processes, such as arthritis and metastasis. Most MMP's are secreted as inactive proproteins which are activated when cleaved by extracellular proteinases. The protein encoded by this gene cleaves type II collagen more efficiently than types I and III. It may be involved in articular cartilage turnover and cartilage pathophysiology associated with osteoarthritis. The gene is part of a cluster of MMP genes which localize to chromosome 11q22.3. [provided by RefSeq, Jul 2008]
Uniprot Description
MMP13: Degrades collagen type I. Does not act on gelatin or casein. Could have a role in tumoral process. Defects in MMP13 are the cause of spondyloepimetaphyseal dysplasia Missouri type (SEMD-MO). A bone disease characterized by moderate to severe metaphyseal changes, mild epiphyseal involvement, rhizomelic shortening of the lower limbs with bowing of the femora and/or tibiae, coxa vara, genu varum and pear-shaped vertebrae in childhood. Epimetaphyseal changes improve with age. Defects in MMP13 are the cause of metaphyseal anadysplasia type 1 (MANDP1). Metaphyseal anadysplasia consists of an abnormal bone development characterized by severe skeletal changes that, in contrast with the progressive course of most other skeletal dysplasias, resolve spontaneously with age. Clinical characteristics are evident from the first months of life and include slight shortness of stature and a mild varus deformity of the legs. Patients attain a normal stature in adolescence and show improvement or complete resolution of varus deformity of the legs and rhizomelic micromelia. Belongs to the peptidase M10A family.
Protein type: Secreted; Secreted, signal peptide; EC 3.4.24.-; Protease
Chromosomal Location of Human Ortholog: 11q22.3
Cellular Component: proteinaceous extracellular matrix; extracellular space; extracellular region
Molecular Function: collagen binding; zinc ion binding; metalloendopeptidase activity; calcium ion binding
Biological Process: collagen catabolic process; extracellular matrix disassembly; extracellular matrix organization and biogenesis; cellular protein metabolic process; proteolysis; bone mineralization; endochondral ossification
Disease: Spondyloepimetaphyseal Dysplasia, Missouri Type