SPARC related modular calcium binding 1 (SMOC1) is an extracellular glycoprotein belonging to the SPARC family. It is localized and secreted in bone marrow derived mesenchymal stem cells (BMSCs) stimulated with osteogenic medium (OSM). The protein is expressed in the developing optic stalk, ventral optic cup, and limbs of mouse embryos. It is composed of five domains, an N-terminal follistatin-like (FS) domain, two thyroglobulin-like (TY) domains similar to SMOC, and an extracellular calcium-binding (EC) domain.
Immunogen
SMOC1 (NP_071420, 150 a.a. ~ 221 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.
SMOC1 plays an essential role in ocular and limb development. It participates in the regulation of cell-matrix interaction by binding to many cell-surface receptors, the extracellular matrix, growth factors, and cytokines. It also functions in bone morphogenetic proteins (BMP) signaling cascade. Mutation in SMOC1 causes a rare autosomal-recessive disorder, microphthalmia and limb anomalies (MLA).
Physical form
Solution in phosphate buffered saline, pH 7.4
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American journal of human genetics, 88(1), 30-41 (2011-01-05)
Microphthalmia with limb anomalies (MLA) is a rare autosomal-recessive disorder, presenting with anophthalmia or microphthalmia and hand and/or foot malformation. We mapped the MLA locus to 14q24 and successfully identified three homozygous (one nonsense and two splice site) mutations in
Journal of proteome research, 9(6), 2946-2956 (2010-04-03)
Extracellular matrix proteins have been implicated in the regulation of osteoblast differentiation of bone marrow derived mesenchymal stem cells (BMSCs) through paracrine or autocrine mechanisms. In the current study, we analyzed the secretory protein profiles of BMSCs grown in osteogenic
American journal of human genetics, 88(1), 92-98 (2011-01-05)
Waardenburg anophthalmia syndrome, also known as microphthalmia with limb anomalies, ophthalmoacromelic syndrome, and anophthalmia-syndactyly, is a rare autosomal-recessive developmental disorder that has been mapped to 10p11.23. Here we show that this disease is heterogeneous by reporting on a consanguineous family, not
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