gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 13 Nov 2015.

SMAD family member 2

The protein encoded by this gene belongs to the SMAD, a family of proteins similar to the gene products of the Drosophila gene 'mothers against decapentaplegic' (Mad) and the C. elegans gene Sma. SMAD proteins are signal transducers and transcriptional modulators that mediate multiple signaling pathways. This protein mediates the signal of the transforming growth factor (TGF)-beta, and thus regulates multiple cellular processes, such as cell proliferation, apoptosis, and differentiation. This protein is recruited to the TGF-beta receptors through its interaction with the SMAD anchor for receptor activation (SARA) protein. In response to TGF-beta signal, this protein is phosphorylated by the TGF-beta receptors. The phosphorylation induces the dissociation of this protein with SARA and the association with the family member SMAD4. The association with SMAD4 is important for the translocation of this protein into the nucleus, where it binds to target promoters and forms a transcription repressor complex with other cofactors. This protein can also be phosphorylated by activin type 1 receptor kinase, and mediates the signal from the activin. Alternatively spliced transcript variants encoding the same protein have been observed. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: TGF-beta, Smad3, V1a, Smad4, CAN
Papers using Smad2 antibodies
Nuclear factor I-C links platelet-derived growth factor and transforming growth factor beta1 signaling to skin wound healing progression.
Lee Sean Bong, In PLoS ONE, 2008
... Rabbit anti-p-Smad3 and total Smad2/3 antibodies were purchased from Cell Signaling Technology (Danvers, MA) ...
GADD34-PP1c recruited by Smad7 dephosphorylates TGF type I receptor.
Goumans Marie Jose, In PLoS ONE, 2003
... The antibodies used were as follows: anti-phospho-Smad2 (Ser465/467) (138D4) and anti-Smad2 (L16D3) antibodies were purchased from Cell Signaling.
The emerging role of lysophosphatidic acid in cancer
Quaranta Vito et al., In Journal of Oncology, 2002
... Polyclonal antibody (pAb) against phosphorylated Smad2 (Ser465/467), GAPDH, and monoclonal antibody (mAb) against Smad2/3 were purchased from Cell Signaling Technology (Danvers, MA), BD ...
Hmg-CoA reductase inhibitor modulates monocyte-endothelial cell interaction under physiological flow conditions in vitro: involvement of Rho GTPase-dependent mechanism
Kim Jae Ho et al., In Experimental & Molecular Medicine, 2000
... Anti-phospho-Smad2 (Ser465/467) and anti-Smad2 antibodies were obtained from Cell Signaling Technology (Beverly, MA) ...
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 ...
more suppliers
Papers on Smad2
Cytoplasmic PML promotes TGF-β-associated epithelial-mesenchymal transition and invasion in prostate cancer.
Regad et al., Derby, United Kingdom. In Oncogene, 09 Dec 2015
This event is associated with activation of TGF-β canonical signalling pathway through the induction of Sma and Mad related family 2 and 3 (SMAD2 and SMAD3) phosphorylation.
Hoxc13 is a crucial regulator of murine hair cycle.
Wu et al., Chongqing, China. In Cell Tissue Res, 09 Dec 2015
At the molecular level, the expression of phosphorylated smad2 (p-smad2), a key factor of active TGF-β1 signaling, was up-regulated in the ShHoxc13-treated hair follicles and down-regulated in rhHoxc13-treated hair follicles, suggesting that Hoxc13 might block anagen-catagen transition by inhibiting the TGF-β1 signaling.
CCN4/WISP-1 positively regulates chondrogenesis by controlling TGF-β3 function.
Kuboki et al., Okayama, Japan. In Bone, 07 Dec 2015
Overexpression of CCN4 enhanced TGF-β3-induced SMAD2/3 phosphorylation and chondrogenesis of hBMSCs in an in vitro assay using a micromass culture model.
Cardiac stem cells transplantation enhances the expression of connexin-43 via the ANG II/AT1R/TGF-beta1 signaling pathway in a rat model of myocardial infarction.
Wang et al., Guangzhou, China. In Exp Mol Pathol, 07 Dec 2015
The expression of mothers against decapentaplegic homolog (SMAD) proteins including SMAD2 and SMAD3 was attenuated whereas SMAD7 was elevated (P < 0.01, P < 0.01, P < 0.05).
Kaposi's Sarcoma-Associated Herpesvirus (KSHV) Induces the Oncogenic miR-17-92 Cluster and Down-Regulates TGF-β Signaling.
Renne et al., Gainesville, United States. In Plos Pathog, 30 Nov 2015
We demonstrate that vFLIP and vCyclin induce the expression of the miR-17-92 cluster to strongly inhibit the TGF-β signaling pathway by down-regulating SMAD2.
Myostatin is a direct regulator of osteoclast differentiation and its inhibition reduces inflammatory joint destruction in mice.
Pap et al., Münster, Germany. In Nat Med, Sep 2015
Myostatin strongly accelerates receptor activator of nuclear factor κB ligand (RANKL)-mediated osteoclast formation in vitro through transcription factor SMAD2-dependent regulation of nuclear factor of activated T-cells (NFATC1).
Marek's disease: Genetic regulation of gallid herpesvirus 2 infection and latency.
Muylkens et al., Namur, Belgium. In Vet J, Sep 2015
Inhibition of expression of the pro-apoptotic factors JARID2 and SMAD2 by viral microRNAs may promote the survival and proliferation of GaHV-2 latently infected cells, thus enhancing tumorigenesis, while inhibition of interleukin 18 by viral microRNAs may be involved in evasion of immune surveillance.
GDF11 Increases with Age and Inhibits Skeletal Muscle Regeneration.
Glass et al., Cambridge, United States. In Cell Metab, Aug 2015
Mechanistically, GDF11 and myostatin both induce SMAD2/3 phosphorylation, inhibit myoblast differentiation, and regulate identical downstream signaling.
β-Catenin Regulates Primitive Streak Induction through Collaborative Interactions with SMAD2/SMAD3 and OCT4.
Semb et al., Copenhagen, Denmark. In Cell Stem Cell, Jul 2015
β-catenin occupies regulatory regions in numerous PS and neural crest genes, and direct interactions between β-catenin and the Nodal effectors SMAD2/SMAD3 are required at these regions for PS gene activation.
Clinical development of galunisertib (LY2157299 monohydrate), a small molecule inhibitor of transforming growth factor-beta signaling pathway.
Lahn et al., Bad Homburg vor der Höhe, Germany. In Drug Des Devel Ther, Dec 2014
Galunisertib (LY2157299 monohydrate) is an oral small molecule inhibitor of the TGF-β receptor I kinase that specifically downregulates the phosphorylation of SMAD2, abrogating activation of the canonical pathway.
Megakaryocytes maintain homeostatic quiescence and promote post-injury regeneration of hematopoietic stem cells.
Li et al., Kansas City, United States. In Nat Med, Nov 2014
MK ablation led to reduced levels of biologically active TGF-β1 protein in the bone marrow and nuclear-localized phosphorylated SMAD2/3 (pSMAD2/3) in HSCs, suggesting that MKs maintain HSC quiescence through TGF-β-SMAD signaling.
New tricks for an old fox: impact of TGFβ on the DNA damage response and genomic stability.
Cucinotta et al., New York City, United States. In Sci Signal, Oct 2014
Recent studies have shown that SMAD2 and SMAD7 participate in the DDR in a manner dependent on ATM or TGFβ receptor type I, respectively, in human fibroblasts and epithelial cells.
The genetic basis of pulmonary arterial hypertension.
Chung et al., New York City, United States. In Hum Genet, May 2014
CAV1 regulates SMAD2/3 phosphorylation, and mutations in CAV1 are a rare cause of PAH.
Molecular mechanisms of FK506-induced hypertension in solid organ transplantation patients.
Zuo et al., Changsha, China. In Chin Med J (engl), 2013
Second, transforming growth factor receptor/SMAD2/3 signaling activation plays an important role in Treg/Th17 cell imbalance in T cells which toget converge to cause inflammation, endothelial dysfunction, and hypertension following tacrolimus treatment.
De novo mutations in histone-modifying genes in congenital heart disease.
Lifton et al., New Haven, United States. In Nature, 2013
There are also two de novo mutations in SMAD2, which regulates H3K27 methylation in the embryonic left-right organizer.
Smad2 decelerates re-epithelialization during gingival wound healing.
Takashiba et al., Okayama, Japan. In J Dent Res, 2012
results indicated Smad2 has inhibitory effects in regulating keratinocyte migration during gingival wound healing. TGF-beta/Smad2 signaling mediating alteration of K16 expression must be tightly regulated during periodontal regeneration.
Post-translational regulation of TGF-β receptor and Smad signaling.
Derynck et al., San Francisco, United States. In Febs Lett, 2012
TGF-beta family signaling through Smads is conceptually a simple and linear signaling pathway, driven by sequential phosphorylation, with type II receptors activating type I receptors, which in turn activate R-Smads [review]
Dynamics of TGF-β/Smad signaling.
Liu et al., Freiburg, Germany. In Febs Lett, 2012
analysis of the dynamics of TGF-beta and Smad2/Smad3 signaling [review]
Smad2/Smad3 in endothelium is indispensable for vascular stability via S1PR1 and N-cadherin expressions.
Kato et al., Tsukuba, Japan. In Blood, 2012
Smad2/3 signaling in ECs is indispensable for maintenance of vascular integrity via the fine-tuning of N-cadherin, VE-cadherin, and S1PR1 expressions in the vasculature.
R-Smad competition controls activin receptor output in Drosophila.
O'Connor et al., Minneapolis, United States. In Plos One, 2011
Data show that dSmad2 directly influences Baboon's phosphorylation of Mad.
More papers using Smad2 antibodies
Alpha 3 beta 1 adhesion to laminin-5 and invasin: critical and differential role of integrin residues clustered at the boundary between alpha 3 N-terminal repeats 2 and 3
Chapman Harold A. et al., In The Journal of Cell Biology, 1998
... Secondary HRP-conjugated antibodies and Smad2/3 pAb were purchased from Santa Cruz Biotechnology, Inc ...
Krox-20 inhibits Jun-NH2-terminal kinase/c-Jun to control Schwann cell proliferation and death
Jessen Kristjan R. et al., In The Journal of Cell Biology, 1998
... Antibody against c-Jun and SMAD2 were purchased from BD Biosciences.
Activin receptors: cellular signalling by receptor serine kinases
Hamada Hiroshi et al., In The Journal of Cell Biology, 1995
... ten Dijke, Leiden University Medical Center, Leiden, Netherlands), rabbit monoclonal antibodies to p-Smad2 (Cell Signaling Technology), and Alexa Fluor ...
share on facebooktweetadd +1mail to friends