Recombinant Mouse Bone Morphogenetic Protein Receptor Type IA

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Recombinant Mouse Bone Morphogenetic Protein Receptor Type IA

Recombinant Mouse Bone Morphogenetic mass is 55-60&120 kDa. Protein Receptor Type IA/Activin Purity Receptor-like Kinase 3 , C-Fc-6His, Human cells Greater than 95% as determined by reducing SDS-PAGE. Source #C520349 Storage: -20°C Package:10 μg/50 μg Human Cells. Physical Appearance This product is only used for scientific Sterile Filtered White lyophilized (freeze-dried) powder. research. It can not be used in medical Formulation treatment or diagnostic procedure for people or animals. It can not be used as food, cosmetics or Lyophilized from a 0.2 μm filtered solution of 20mM PB, 150 household products. No one may manufacture, mM NaCl, pH 7.4. promise to sell, import, or use all relevant patents and Endotoxin trademarks of a product without authorization or approval in writing. If you need permission for other Less than 0.1 ng/µg (1 EU/µg) as determined by LAL test. uses, please contact us or visit our website. You must Reconstitution comply with all applicable licensing requirements on the product page when using this product. It is your Dissolve the lyophilized protein in distilled water. responsibility to read, understand and comply with all Background provisos of this kind. ALK-3 is a type I receptor for bone morphogenetic proteins (BMPs) which belong to the protein kinase superfamily, TKL Description Ser/Thr protein kinase family and TGFB receptor subfamily. Recombinant Mouse Bone Morphogenetic Protein Receptor The BMP receptors consists of the type I receptors BMPR1A Type IA/Activin Receptor-like Kinase 3 is produced by our and BMPR1B and the type I I receptor BMPR2. Seven known Mammalian expression system and the target gene encoding type I serine/threonine kinases and five mammalian type II Gln24-Arg152 is expressed with a Fc, 6His tag at the serine/threonine kinase receptors function in TGF-beta C-terminus. superfamily signal transduction. The downstream molecules of the type I BMP receptors include the Smad (Smad1, 5 and Storage 8) proteins that are phosphorylated in a ligand-dependent Lyophilized protein should be stored at < -20°C, though stable manner, and relay the BMP signal from the receptors to target at room temperature for 3 weeks.Reconstituted protein genes in the nucleus. Type II receptors phosphorylate and solution can be storedS at 4-7angon°C for 2-7 days.Aliquots of a ctivBiate type I roeceptorts wehich auchtophosphorylate, then bind reconstituted samples are stable at < -20°C for 3 months. and activate SMAD transcriptional regulators. ALK-3 contains a GS domain and a protein kinase domain. ALK-3 is widely Usage expressed. Defects in BMPR1A gene are a cause of a This material is offered by Sangon Biotech for research, significant proportion of cases of Juvenile polyposis laboratory or further evaluation purposes. NOT FOR HUMAN syndrome (JPS). USE. Accession Molecular Weight P36895. The theoretical molecular mass is 42.2 kDa, AP molecular .

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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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