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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

SMAD family member 9

The protein encoded by this gene is a member of the SMAD family, which transduces signals from TGF-beta family members. The encoded protein is activated by bone morphogenetic proteins and interacts with SMAD4. Two transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Jan 2010] (from NCBI)
Top mentioned proteins: Smad1, Smad5, Smad4, BMPR1A, Smad2
Papers on Smad8
Smad1/5/8 are myogenic regulators of murine and human mesoangioblasts.
Sampaolesi et al., Torino, Italy. In J Mol Cell Biol, Feb 2016
Similarly, siRNA-mediated knockdown of Smad8 in Smad1/5-null MABs or inhibition of SMAD1/5/8 phosphorylation with Dorsomorphin (DM) also improved myogenic differentiation, demonstrating a novel role of SMAD8.
Antagonism of the met5-enkephalin-opioid growth factor receptor-signaling axis promotes MSC to differentiate into osteoblasts.
Margulies et al., In J Orthop Res, Jan 2016
Importantly, SMAD1 and SMAD8/9 expression increased after a pulse dose of naloxone while SMAD1, SMAD7 and ID1 were increased in the OGFR deficient MSC.
Bone Morphogenetic Protein-6 (BMP-6) Stimulates the Antrum Formation by the Regulation of its Signalling Pathway in Caprine Pre-antral Follicles Cultured In Vitro.
Figueiredo et al., Fortaleza, Brazil. In Reprod Domest Anim, Jan 2016
Thus, this study investigated the effect of bone morphogenetic protein (BMP-6) and recombinant follicle-stimulating hormone (rFSH) alone or in combination on the in vitro culture (IVC) of isolated caprine secondary follicles (Experiment 1) and the mRNA levels for BMP receptors/Smad signalling pathway (BMPR1A, BMPR2, SMAD1, SMAD4, SMAD5, SMAD6, SMAD7 and SMAD8) in vivo and in vitro using BMP-6 (Experiment 2).
Heterozygous Mutations in BMP6 Pro-peptide Lead to Inappropriate Hepcidin Synthesis and Moderate Iron Overload in Humans.
Tchernitchko et al., Paris, France. In Gastroenterology, Dec 2015
In cell lines, the mutated residues in the BMP6 propeptide resulted in defective secretion of BMP6; reduced signaling via SMAD1, SMAD5, and SMAD8; and loss of hepcidin production.
The BMP signaling pathway leads to enhanced proliferation in serous ovarian cancer-a potential therapeutic target.
Konishi et al., Kyoto, Japan. In Mol Carcinog, Mar 2015
SMAD2 and SMAD3 mediate TGF-β signaling, whereas SMAD1, SMAD5, and SMAD8/9 transduce bone morphogenetic protein (BMP) signals.
trans-10,cis-12 CLA promotes osteoblastogenesis via SMAD mediated mechanism in bone marrow mesenchymal stem cells.
Park et al., Amherst Center, United States. In J Funct Foods, 2014
Thus the purpose of this study was to determine involvement of CLA on regulation of osteoblastogenesis in murine mesenchymal stem cells by focusing on the Mothers against decapentaplegic (MAD)-related family of molecules 8 (SMAD8), one of key regulators of osteoblastogenesis.
Recurrent somatic mutations in ACVR1 in pediatric midline high-grade astrocytoma.
Kieran et al., Montréal, Canada. In Nat Genet, 2014
Hyperactivation of the bone morphogenetic protein (BMP)-ACVR1 developmental pathway in mHGAs harboring ACVR1 mutations led to increased levels of phosphorylated SMAD1, SMAD5 and SMAD8 and upregulation of BMP downstream early-response genes in tumor cells.
The genetic basis of pulmonary arterial hypertension.
Chung et al., New York City, United States. In Hum Genet, 2014
Mutations in ALK-1, ENG, SMAD4 and SMAD8, other TGFβ family members, are additional rare causes of PAH.
Bone morphogenetic protein 2 stimulates noncanonical SMAD2/3 signaling via the BMP type 1A receptor in gonadotrope-like cells: implications for FSH synthesis.
Bernard et al., Montréal, Canada. In Endocrinology, 2014
These data challenge current dogma that ALK3 and other BMP type I receptors signal via SMAD1, SMAD5, and SMAD8 and not SMAD2 or SMAD3.
Inhibition of mTORC1 kinase activates Smads 1 and 5 but not Smad8 in human prostate cancer cells, mediating cytostatic response to rapamycin.
Danielpour et al., Cleveland, United States. In Mol Cancer Res, 2012
Data suggest that Smads 1, 5 and 8 as potential prognostic markers and therapeutic targets for mTOR inhibition therapy of prostate cancer.
Missense mutations of the BMPR1B (ALK6) gene in childhood idiopathic pulmonary arterial hypertension.
Nakanishi et al., Tokorozawa, Japan. In Circ J, 2011
BACKGROUND: Mutations in the bone morphogenetic protein receptor type 2 (BMPR2) gene, the activin receptor-like kinase 1 (ALK1) gene, and SMAD8 gene have been reported in heritable pulmonary arterial hypertension (HPAH) and in idiopathic pulmonary arterial hypertension (IPAH).
Biomechanical forces exert anabolic effects on osteoblasts by activation of SMAD 1/5/8 through type 1 BMP receptor.
Agarwal et al., Regensburg, Germany. In Biorheology, 2010
biomechanical stimulation of osteoblasts activates SMAD 1/5/8 in the BMP signaling pathway through BMPR1 and may enhance osteogenesis by upregulating SMAD-dependent osteogenic genes
Hemodynamic and clinical onset in patients with hereditary pulmonary arterial hypertension and BMPR2 mutations.
Grünig et al., Heidelberg, Germany. In Respir Res, 2010
In non-carriers with familial aggregation of PAH further genes/gene regions as the BMPR2 promoter region, the ACVRL1, Endoglin, and SMAD8 genes have been analysed.
ALK5 phosphorylation of the endoglin cytoplasmic domain regulates Smad1/5/8 signaling and endothelial cell migration.
Blobe et al., Durham, United States. In Carcinogenesis, 2010
ALK5 phosphorylates endoglin on Ser 646 & 649 in endothelial cells. Losing pSer646 prevents inhibition of TGF-beta-induced Smad1/5/8 signaling & cell migration. Losing both pSer646 & pSer649 prevents inhibition of BMP-9-mediated Smad1/5/8 signaling.
Endoglin is involved in BMP-2-induced osteogenic differentiation of periodontal ligament cells through a pathway independent of Smad-1/5/8 phosphorylation.
Kawashima et al., Tokyo, Japan. In J Cell Physiol, 2010
Endoglin is involved in BMP-2-induced osteogenic differentiation of periodontal ligament cells through a pathway independent of Smad-1/5/8 phosphorylation.
Characterization of mammary epithelial cell line HC11 using the NIA 15k gene array reveals potential regulators of the undifferentiated and differentiated phenotypes.
Shemanko et al., Calgary, Canada. In Differentiation, 2009
Although the amounts of bone morphogenetic protein receptor-1A (BMPR1A) protein were present at all stages, we found the activity of its downstream signal transduction pathway, as measured by the presence of phosphorylated-SMAD1, -SMAD5, and -SMAD8, is elevated in undifferentiated cells and decreases in fully differentiated cells.
Defective pulmonary vascular remodeling in Smad8 mutant mice.
Martin et al., Houston, United States. In Hum Mol Genet, 2009
Smad8 loss of function resulted in changes in pulmonary arteries including medial thickening and smooth muscle hyperplasia observed in patients with pulmonary artery hypertension.
A new nonsense mutation of SMAD8 associated with pulmonary arterial hypertension.
Matsuoka et al., Tokyo, Japan. In J Med Genet, 2009
Study described the first mutation in SMAD8 in a patient with IPAH, and suggested the involvement of SMAD8 in the pathogenesis of PAH.
BMP type I receptor inhibition reduces heterotopic [corrected] ossification.
Bloch et al., In Nat Med, 2008
6), inhibits activation of the BMP signaling effectors SMAD1, SMAD5 and SMAD8 in tissues expressing caALK2 induced by adenovirus specifying Cre (Ad.Cre).
Molecular detection of smad2/smad4 alterations in colorectal tumors.
Thiagalingam, Boston, United States. In Methods Mol Med, 2000
Table 1 Human SMAD Genes and Cancers Gene Map position Affected cancers Reference(s) SMAD1 4q28-31 None 24 SMAD2 18q21 Colon 24 , 26 , 32 SMAD3 15q21-22 None 24 , 33 SMAD4 18q21 Lung, pancreatic,and colon 22-25 , 33 SMAD5 5q31 None 24 , 33 SMAD6 15q21-22 None 24 , 33 SMAD7 18q21 None 24 , 33 , 34 SMAD8/MADH6 13q12-14 None 35.
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