BMP Receptor IA Recombinant Protein Cat

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BMP receptor IA Recombinant Protein Cat. No.: 91-930 BMP receptor IA Recombinant Protein Specifications SPECIES: Human SOURCE SPECIES: Human Cells SEQUENCE: Gln24-Arg152 FUSION TAG: C-Fc-6 His tag TESTED APPLICATIONS: APPLICATIONS: This recombinant protein can be used for biological assays. For research use only. PREDICTED MOLECULAR 42.1 kD WEIGHT: Properties Greater than 95% as determined by reducing SDS-PAGE. PURITY: Endotoxin level less than 0.1 ng/ug (1 IEU/ug) as determined by LAL test. PHYSICAL STATE: Lyophilized Lyophilized from a 0.2 um filtered solution of PBS, pH 7.4. It is not recommended to BUFFER: reconstitute to a concentration less than 100 ug/ml. Dissolve the lyophilized protein in ddH2O. September 24, 2021 1 https://www.prosci-inc.com/bmp-receptor-ia-recombinant-protein-91-930.html Lyophilized protein should be stored at -20˚C, though stable at room temperature for 3 weeks. STORAGE CONDITIONS: Reconstituted protein solution can be stored at 4-7˚C for 2-7 days. Aliquots of reconstituted samples are stable at -20˚C for 3 months. Additional Info OFFICIAL SYMBOL: BMPR1A Bone Morphogenetic Protein Receptor Type-1A, BMP Type-1A Receptor, BMPR-1A, Activin ALTERNATE NAMES: Receptor-Like Kinase 3, ALK-3, Serine/Threonine-Protein Kinase Receptor R5, SKR5, CD292, BMPR1A, ACVRLK3, ALK3 ACCESSION NO.: P36894 GENE ID: 657 Background and References Bone Morphogenetic Protein Receptor Type-1A (BMPR1A) belongs to the TKL Ser/Thr protein kinase family and TGFB receptor subfamily, including the type I receptors BMPR1A and BMPR1B and the type II receptor BMPR2. BMPR1A is a single-pass type I membrane protein and highly expressed in skeletal muscle. BMPR1A contains one GS domain and BACKGROUND: one protein protein kinase domain. BMPR1A is necessary for the extracellular matrix depostition by osteoblasts. BMPR1A can activate SMAD transcriptional regulators, binding with ligands. Defects in BMPR1A are a cause of juvenile polyposis syndrome, Cowden disease and hereditary mixed polyposis syndrome 2 (HMPS2). ANTIBODIES FOR RESEARCH USE ONLY. For additional information, visit ProSci's Terms & Conditions Page. September 24, 2021 2 https://www.prosci-inc.com/bmp-receptor-ia-recombinant-protein-91-930.html.

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The Prevalence of MADH4 and BMPR1A Mutations in Juvenile Polyposis and Absence of BMPR2, BMPR1B, and ACVR1 Mutations
484 ORIGINAL ARTICLE J Med Genet: first published as 10.1136/jmg.2004.018598 on 2 July 2004. Downloaded from The prevalence of MADH4 and BMPR1A mutations in juvenile polyposis and absence of BMPR2, BMPR1B, and ACVR1 mutations J R Howe, M G Sayed, A F Ahmed, J Ringold, J Larsen-Haidle, A Merg, F A Mitros, C A Vaccaro, G M Petersen, F M Giardiello, S T Tinley, L A Aaltonen, H T Lynch ............................................................................................................................... J Med Genet 2004;41:484–491. doi: 10.1136/jmg.2004.018598 Background: Juvenile polyposis (JP) is an autosomal dominant syndrome predisposing to colorectal and gastric cancer. We have identified mutations in two genes causing JP, MADH4 and bone morphogenetic protein receptor 1A (BMPR1A): both are involved in bone morphogenetic protein (BMP) mediated signalling and are members of the TGF-b superfamily. This study determined the prevalence of mutations See end of article for in MADH4 and BMPR1A, as well as three other BMP/activin pathway candidate genes in a large number authors’ affiliations ....................... of JP patients. Methods: DNA was extracted from the blood of JP patients and used for PCR amplification of each exon of Correspondence to: these five genes, using primers flanking each intron–exon boundary. Mutations were determined by Dr J R Howe, Department of Surgery, 4644 JCP, comparison to wild type sequences using sequence analysis software. A total of 77 JP cases were University of Iowa College sequenced for mutations in the MADH4, BMPR1A, BMPR1B, BMPR2, and/or ACVR1 (activin A receptor) of Medicine, 200 Hawkins genes. The latter three genes were analysed when MADH4 and BMPR1A sequencing found no mutations.
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