gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 12 Nov 2015.

SMAD family member 4

Smad4, DPC4
This gene encodes a member of the Smad family of signal transduction proteins. Smad proteins are phosphorylated and activated by transmembrane serine-threonine receptor kinases in response to TGF-beta signaling. The product of this gene forms homomeric complexes and heteromeric complexes with other activated Smad proteins, which then accumulate in the nucleus and regulate the transcription of target genes. This protein binds to DNA and recognizes an 8-bp palindromic sequence (GTCTAGAC) called the Smad-binding element (SBE). The Smad proteins are subject to complex regulation by post-translational modifications. Mutations or deletions in this gene have been shown to result in pancreatic cancer, juvenile polyposis syndrome, and hereditary hemorrhagic telangiectasia syndrome. [provided by RefSeq, Oct 2009] (from NCBI)
Top mentioned proteins: p53, HAD, CAN, p16, TGF-beta
Papers using Smad4 antibodies
Smad4 is required for the normal organization of the cartilage growth plate
Glimcher Laurie H et al., In The EMBO Journal, 2004
... (Santa Cruz); anti-Smad2, anti-phospho-Smad1/5/8, anti-phospho-Smad2 (S465/467), and anti-phospho-p38 (Cell Signaling); anti-Smad1 (Invitrogen); anti-Flag (M2, Sigma); anti-Smad4 (Abcam); anti-XIAP (Stressgen); and anti-GAPDH ...
Transforming growth factor-beta-induced inhibition of myogenesis is mediated through Smad pathway and is modulated by microtubule dynamic stability
Kapus András et al., In The Journal of Cell Biology, 2003
tubulin (Sigma-Aldrich), cofilin, Smad2, phospho-Smad3, Smad4 (Cell Signaling Technology), c-Myc (clone 9E10), ...
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.
Nurminsky Dmitry I., In PLoS ONE, 2002
... ab65252), HDAC4 (Cell Signaling, #2072), HAND2 (Abcam, ab56590), Tropomyosin C (Santacruz, sc73225), DnaJB1 (Santacruz, sc-1800) and SMAD4 (Abcam, ab1341) ...
CHMP5 is essential for late endosome function and down-regulation of receptor signaling during mouse embryogenesis
Ghosh Sankar et al., In The Journal of Cell Biology, 1999
... The antibodies used were anti–phospho-Erk1/2 (Cell Signaling Technology), anti–phospho-Smad2 (Cell Signaling Technology), anti-Smad4 (Santa Cruz Biotechnology, Inc; H552), anti-Smad2 (Cell ...
Regulation of growth and prostatic marker expression by activin A in an androgen-sensitive prostate cancer cell line LNCAP
Nishio K et al., 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- ...
Papers on Smad4
Next-Generation Sequencing of Matched Primary and Metastatic Rectal Adenocarcinomas Demonstrates Minimal Mutation Gain and Concordance to Colonic Adenocarcinomas.
Portier et al., Houston, United States. In Arch Pathol Lab Med, 04 Dec 2015
The mutations identified, listed in order of frequency, included TP53, KRAS, APC, FBXW7, GNAS, FGFR3, BRAF, NRAS, PIK3CA, and SMAD4.
microRNA for determining the age-related myogenic capabilities of skeletal muscle.
Kwon et al., Taejŏn, South Korea. In Bmb Rep, 02 Dec 2015
We found that miR-431 directly binds to 3`untranslated regions (UTR) of Smad4 mRNA, and decreases its expression.
Identification of gene markers in the development of smoking-induced lung cancer.
Wang et al., Wuhan, China. In Gene, 27 Nov 2015
Importantly, MAPK1 (degree =30), SRC (degree =29), SMAD4 (degree =23), EEF1A1 (degree =21), TRAF2 (degree =21) and PLCG1 (degree =20) had higher degrees in the PPI network of the DEGs.
RAS signaling and anti-RAS therapy: lessons learned from genetically engineered mouse models, human cancer cells, and patient-related studies.
Fang, Houston, United States. In Acta Biochim Biophys Sin (shanghai), 07 Oct 2015
Studies on clinical specimens also demonstrated that KRAS mutations are present in premalignant tissues and that most of KRAS mutant human cancers have co-mutations in other cancer driver genes, including TP53, STK11, CDKN2A, and KMT2C in lung cancer; APC, TP53, and PIK3CA in colon cancer; and TP53, CDKN2A, SMAD4, and MED12 in pancreatic cancer.
From Barrett metaplasia to esophageal adenocarcinoma: the molecular background.
Rugge et al., Padova, Italy. In Histol Histopathol, 03 Oct 2015
Recent comprehensive mutational profiling studies identified that the inactivation of the TP53 and of the SMAD4 tumour suppressor genes occurred in a stage-specific manner, confined to (high grade) dysplastic and neoplastic lesions, respectively.
Stem vs non-stem cell origin of colorectal cancer.
Sansom et al., Glasgow, United Kingdom. In Br J Cancer, Jul 2015
The progression of this cancer from an early adenoma to carcinoma is accompanied by a well-characterised set of mutations including KRAS, SMAD4 and TP53.
It's a SMAD/SMAD World.
Maitra et al., Houston, United States. In Cell, Jul 2015
DPC4/SMAD4 mutations are associated with aggressive pancreatic cancer.
[Advance in the biology of pancreatic of cancer].
Cordelier et al., Toulouse, France. In Bull Cancer, Jun 2015
P16, TP53, DPC4/Smad4 tumor suppressor pathways are genetically inactivated in the majority of pancreatic carcinomas, whereas oncogenic k-ras is activated.
Sequential cancer mutations in cultured human intestinal stem cells.
Clevers et al., Utrecht, Netherlands. In Nature, Jun 2015
Here we utilize CRISPR/Cas9 technology for targeted gene modification of four of the most commonly mutated colorectal cancer genes (APC, P53 (also known as TP53), KRAS and SMAD4) in cultured human intestinal stem cells.
Modeling colorectal cancer using CRISPR-Cas9-mediated engineering of human intestinal organoids.
Sato et al., Tokyo, Japan. In Nat Med, Mar 2015
By modulating the culture conditions to mimic that of the intestinal niche, we selected isogenic organoids harboring mutations in the tumor suppressor genes APC, SMAD4 and TP53, and in the oncogenes KRAS and/or PIK3CA.
Whole genomes redefine the mutational landscape of pancreatic cancer.
Grimmond et al., Brisbane, Australia. In Nature, 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).
Genetic diagnosis of high-penetrance susceptibility for colorectal cancer (CRC) is achievable for a high proportion of familial CRC by exome sequencing.
Houlston et al., London, United Kingdom. In J Clin Oncol, Mar 2015
PATIENTS AND METHODS: To quantify the impact of germline mutation to familial CRC, we sequenced the mismatch repair genes (MMR) APC, MUTYH, and SMAD4/BMPR1A in 626 early-onset familial CRC cases ascertained through a population-based United Kingdom national registry.
Prediction of response to anti-EGFR antibody-based therapies by multigene sequencing in colorectal cancer patients.
Negrini et al., Ferrara, Italy. In Bmc Cancer, Dec 2014
In addition, mutations in FBXW7 and SMAD4 were prevalent in cases that were non-responsive to anti-EGFR moAb.
Pancreatic cancer: optimizing treatment options, new, and emerging targeted therapies.
Coveler et al., Seattle, United States. In Drug Des Devel Ther, Dec 2014
Pancreatic adenocarcinoma is characterized by several germline or acquired genetic mutations, the most common being KRAS (90%), CDK2NA (90%), TP53 (75%-90%), DPC4/SMAD4 (50%).
Whole Exome Sequencing of Rapid Autopsy Tumors and Xenograft Models Reveals Possible Driver Mutations Underlying Tumor Progression.
Hidalgo et al., San Diego, United States. In Plos One, Dec 2014
Based on the mutation prevalence in the primary and metastatic sites, we proposed possible clonal evolution patterns marked by functional mutations affecting cancer genes such as KRAS, TP53 and SMAD4 that may play an important role in tumor initiation, progression and metastasis.
MicroRNA-146a modulates TGF-beta1-induced hepatic stellate cell proliferation by targeting SMAD4.
Li et al., Hefei, China. In Cell Signal, 2012
Bioinformatics analyses predict that Smad4 is the potential target of miR-146a.
Vascular smooth muscle cell Smad4 gene is important for mouse vascular development.
Chen et al., Birmingham, United States. In Arterioscler Thromb Vasc Biol, 2012
Provide important insight into the role of Smad4 and its upstream Smads in regulating vascular smooth muscle function and vascular development of mice.
Transforming growth factor-β/SMAD Target gene SKIL is negatively regulated by the transcriptional cofactor complex SNON-SMAD4.
Macías-Silva et al., Mexico. In J Biol Chem, 2012
when the SNON-SMAD4 complex is absent as in some cancer cells lacking SMAD4 the regulation of some TGF-beta target genes is modified
Dynamics of TGF-β signaling reveal adaptive and pulsatile behaviors reflected in the nuclear localization of transcription factor Smad4.
Brivanlou et al., New York City, United States. In Proc Natl Acad Sci U S A, 2012
TGF-beta signaling has a role in nuclear localization of transcription factor Smad4
Mutations of SMAD4 account for both LAPS and Myhre syndromes.
Thibodeau et al., In Am J Med Genet A, 2012
Missense mutations of SMAD4 account for both LAPS and Myhre syndromes.
share on facebooktweetadd +1mail to friends