BMPR1A/ALK-3 Lysate | BMPR1A lysate

Human BMPR1A/ALK-3 HEK293 Overexpression Lysate

Cat. Num. AAA8119625

• Applications: Western Blot
• Synonyms: BMPR1A/ALK-3; Human BMPR1A/ALK-3 HEK293 Overexpression Lysate; Human BMPRIA/ALK-3/CD292 HEK293 Cell Lysate (WB positive control); Human 10q23del Overexpression Lysate; Human ACVRLK3 Overexpression Lysate; Human ALK3 Overexpression Lysate; Human CD292 Overexpression Lysate; Human SKR5 Overexpression Lysate; bone morphogenetic protein receptor; type IA; BMPR1A lysate

• Host: HEK293 Cells
• Form/Format: Modified RIPA Lysis Buffer: 50 mM Tris-HCl pH7.4, 150 mM NaCl, 1mM EDTA, 1% Triton X-100, 0.1% SDS, 1% Sodium deoxycholate, 1mM PMSF.; 1 X Sample Buffer (1 X modified RIPA buffer+1 X SDS loading buffer).

• Applicable Applications for BMPR1A lysate: Western Blot (WB)
• Application Notes: Western blot (WB): Use at an assay dependent dilution.
• Species: Human
• Sequence Information: A DNA sequence encoding the extracellular domain (Met 1-Arg 152) of human ALK3 (NP_004320.2) was fused with a polyhistidine tag at the C-terminus.
• Preparation Method: Cell lysate was prepared by homogenization of the over-expressed cells in ice-cold modified RIPA Lysis Buffer with cocktail of protease inhibitors (Sigma). Cell debris was removed by centrifugation. Protein concentration was determined by Bradford assay (protein assay, Microplate Standard assay). The cell lysate was boiled for 5 min in 1 x SDS loading buffer (50mM Tris-HCl pH6.8, 12.5% glycerol, 1% sodium dodecylsulfate, 0.01% bromophenol blue) containing 5% b-mercaptoethanol, and lyophilized.
• Recommend Usage: 1. Centrifuge the tube for a few seconds and ensure the pellet at the bottom of the tube.; 2. Re-dissolve the pellet using 200uL pure water and boil for 2-5 min.
• Preparation and Storage: Store at 4 degree C for up to twelve months from date of receipt. After re-dissolution, aliquot and store at -80 degree C for up to twelve months. Avoid repeated freeze-thaw cycles.

Related Product Information for BMPR1A lysate

Description: This Human BMPR1A/ALK-3 overexpression lysate was created in HEK293 Cells and intented for use as a Western blot (WB) positive control. Purification of BMPR1A/ALK-3 protein from the overexpression lysate was verified.

Background: Human Cell lysate that Human BMPRIA/ALK-3/CD292 transfected/overexpressed for Western blot (WB) positive control. The whole cell lysate is provided in 1X Sample Buffer (1X modified RIPA buffer+1X SDS loading buffer).
Activin receptor-Like Kinase 3 (ALK-3), also known as Bone Morphogenetic Protein Receptor, type IA (BMPR1A), is a type I receptor for bone morphogenetic proteins (BMPs) which belong to the transforming growth factor beta (TGF-beta) superfamily. The BMP receptors form a subfamily of transmembrane serine/threonine kinases including the type I receptors BMPR1A and BMPR1B and the type II receptor BMPR2. ALK-3/BMPR1A is expressed in the epithelium during branching morphogenesis. Deletion of BMPR1A in the epithelium with an Sftpc-cre transgene leads to dramatic defects in lung development. ALK-3 and ALK-6 share a high degree of homology, yet possess distinct signaling roles. The transforming growth factor (TGF)-beta type III receptor (TbetaRIII) enhanced both ALK-3 and ALK-6 signaling. TbetaRIII associated with ALK-3 primarily through their extracellular domains, whereas its interaction with ALK-6 required both the extracellular and cytoplasmic domains. ALK-3 plays an essential role in the formation of embryonic ventral abdominal wall, and abrogation of BMP signaling activity due to gene mutations in its signaling components could be one of the underlying causes of omphalocele at birth. The type IA BMP receptor, ALK-3 was specifically required at mid-gestation for normal development of the trabeculae, compact myocardium, interventricular septum, and endocardial cushion. Cardiac muscle lacking ALK-3 was specifically deficient in expressing TGFbeta2, an established paracrine mediator of cushion morphogenesis. Hence, ALK-3 is essential, beyond just the egg cylinder stage, for myocyte-dependent functions and signals in cardiac organogenesis.

References

Gaussin V, et al. (2002) Endocardial cushion and myocardial defects after cardiac myocyte-specific conditional deletion of the bone morphogenetic protein receptor ALK3. Proc Natl Acad Sci U S A. 99(5): 2878-83.Eblaghie MC, et al. (2006) Evidence that autocrine signaling through Bmpr1a regulates the proliferation, survival and morphogenetic behavior of distal lung epithelial cells. Dev Biol. 291(1): 67-82.Sun J, et al. (2007) Deficient Alk3-mediated BMP signaling causes prenatal omphalocele-like defect. Biochem Biophys Res Commun. 360(1): 238-43.Lee NY, et al. (2009) The transforming growth factor-beta type III receptor mediates distinct subcellular trafficking and downstream signaling of activin-like kinase (ALK)3 and ALK6 receptors. Mol Biol Cell. 20(20): 4362-70.