Insulin-like growth factor-I inhibits transcriptional responses of transforming growth factor-beta by phosphatidylinositol 3-kinase/Akt-dependent suppression of the activation of Smad3 but not Smad2.
In PLoS ONE, 2002
... ab65252), HDAC4 (Cell Signaling, #2072), HAND2 (Abcam, ab56590), Tropomyosin C (Santacruz, sc73225), DnaJB1 (Santacruz, sc-1800) and SMAD4 (Abcam, ab1341) ... Regulation of growth and prostatic marker expression by activin A in an androgen-sensitive prostate cancer cell line LNCAP
In British Journal of Cancer, 1996
... The following antibodies were used: anti-p21, anti-cdk2, anti-cyclin D, anti-phospho-Rb, anti-Smad2, anti-phospho-Smad2, anti-Smad3, anti-Smad4, and secondary antibodies (Cell Signaling, Beverly, MA, USA); anti- ...
Whole genomes redefine the mutational landscape of pancreatic cancer.
Brisbane, Australia. In Nature, 26 Mar 2015
Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2).
Novel Targets in Pancreatic Cancer Research.
Philadelphia, United States. In Semin Oncol, Feb 2015
For example, PDA is driven by key activating, gain-of-function mutations in proto-oncogenes (eg, K-Ras) along with loss of function of tumor suppressor genes (eg, p16, SMAD4).
Research on potential biomarkers in hereditary hemorrhagic telangiectasia.
Madrid, Spain. In Front Genet, Dec 2014
Hereditary hemorrhagic telangiectasia (HHT) is a genetically heterogeneous disorder, involving mutations in two predominant genes known as Endoglin (ENG; HHT1) and activin receptor-like kinase 1 (ACVRL1/ALK1; HHT2), as well as in some less frequent genes, such as MADH4/SMAD4 (JP-HHT) or BMP9/GDF2 (HHT5).
Diagnosis and molecular aspects of solid-pseudopapillary neoplasms of the pancreas.
Paris, France. In Semin Diagn Pathol, Nov 2014
Distinctive molecular alterations such as the presence of CTNNB1 mutations are observed in nearly all cases, while mutations classically observed in ductal adenocarcinoma, such as KRAS, TP53, and SMAD4, are not observed in SPNs, reinforcing its distinct nature compared to all other pancreatic neoplasms.
Serous cystic neoplasms of the pancreas: clinicopathologic and molecular characteristics.
Atlanta, United States. In Semin Diagn Pathol, Nov 2014
Serous cystadenomas also lack the molecular alterations that characterize ductal neoplasms, such as mutation of KRAS (high prevalence in most mucinous ductal neoplasms), inactivation of SMAD4 (seen in ductal adenocarcinomas), and mutations in GNAS (seen in some IPMNs) and RNF43 (detected in MCNs and IPMNs).