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Smad3 SMAD family member 3 [ Mus musculus (house mouse) ]

Gene ID: 17127, updated on 20-Aug-2014

GeneRIFs: Gene References Into Functions

GeneRIFPubMed TitleDate
miR-433 is an important component of TGF-beta/Smad3-induced renal fibrosis through the induction of a positive feedback loop to amplify TGF-beta/Smad3 signaling.

The microRNA miR-433 promotes renal fibrosis by amplifying the TGF-β/Smad3-Azin1 pathway.
Li R, Chung AC, Dong Y, Yang W, Zhong X, Lan HY.

07/26/2014
Smad3 signaling inhibition rescues muscle regenerative responses and attenuates myostatin/TGFbeta receptor/pSmad3 signaling. in type 1 diabetic mice.

Pharmacological inhibition of myostatin/TGF-β receptor/pSmad3 signaling rescues muscle regenerative responses in mouse model of type 1 diabetes.
Jeong J, Conboy MJ, Conboy IM.

07/19/2014
findings indicate that ERK5 plays a critical role in TGF-beta1-induced pulmonary fibrosis via enhancing Smad3 acetylation.

ERK5 inhibition ameliorates pulmonary fibrosis via regulating Smad3 acetylation.
Kim S, Lim JH, Woo CH.

07/5/2014
Smad3 is sufficient to regulate many of the events associated with myostatin-induced atrophy.

Smad3 induces atrogin-1, inhibits mTOR and protein synthesis, and promotes muscle atrophy in vivo.
Goodman CA, McNally RM, Hoffmann FM, Hornberger TA.,

06/21/2014
Smad3 signaling has an essential role in the activation of bone marrow-derived fibroblasts in the kidney during the pathogenesis of renal fibrosis.

Smad3 signaling activates bone marrow-derived fibroblasts in renal fibrosis.
Chen J, Xia Y, Lin X, Feng XH, Wang Y.,

06/14/2014
Defects in the Smad3 gene may increase susceptibility to the development of septic hypotension because of enhanced iNOS production.

Deficiency of Smad3 results in enhanced inducible nitric oxide synthase-mediated hypotension in lipopolysaccharide-induced endotoxemia.
Lv KY, Zhong QS, Liu XF, Zhu SH, Xiao SC, Wang GY, Ma B, Xia ZF.

05/24/2014
Mstn is a potent inducer of insulin resistance by degrading IRS1 protein via the E3 ligase, Cblb, in a Smad3-dependent manner

Myostatin induces insulin resistance via Casitas B-lineage lymphoma b (Cblb)-mediated degradation of insulin receptor substrate 1 (IRS1) protein in response to high calorie diet intake.
Bonala S, Lokireddy S, McFarlane C, Patnam S, Sharma M, Kambadur R.,

05/17/2014
Data sugggest that Smad3-/- embryonic stem cell cell formed teratomas can therefore provide a new model for the study of the mechanism of malignant teratomas.

Suppression of malignancy by Smad3 in mouse embryonic stem cell formed teratoma.
Li P, Chen Y, Meng X, Kwok KY, Huang X, Choy KW, Wang CC, Lan H, Yuan P.

05/10/2014
Glucocorticoids recruit Tgfbr3 and Smad1 to shift transforming growth factor-beta signaling from the Tgfbr1/Smad2/3 axis to the Acvrl1/Smad1 axis in lung fibroblasts.

Glucocorticoids recruit Tgfbr3 and Smad1 to shift transforming growth factor-β signaling from the Tgfbr1/Smad2/3 axis to the Acvrl1/Smad1 axis in lung fibroblasts.
Schwartze JT, Becker S, Sakkas E, Wujak ŁA, Niess G, Usemann J, Reichenberger F, Herold S, Vadász I, Mayer K, Seeger W, Morty RE.,

04/12/2014
Smad3 is required for the survival of proliferative intermediate progenitor cells in the dentate gyrus of adult mice.

Smad3 is required for the survival of proliferative intermediate progenitor cells in the dentate gyrus of adult mice.
Tapia-González S, Muñoz MD, Cuartero MI, Sánchez-Capelo A., Free PMC Article

02/22/2014
Serine-204 phosphorylation in the Smad3 linker region is a critical event by which ERK enhances Smad3-mediated COL1A2 promoter activity in mesenchymal cells

Serine-204 in the linker region of Smad3 mediates the collagen-I response to TGF-β in a cell phenotype-specific manner.
Browne JA, Liu X, Schnaper HW, Hayashida T.,

02/15/2014
a detailed computational model for TGF-beta signalling that incorporates elements of previous models together with crosstalking between Smad1/5/8 and Smad2/3 channels through a negative feedback loop dependent on Smad7.

Computational modelling of Smad-mediated negative feedback and crosstalk in the TGF-β superfamily network.
Nicklas D, Saiz L.,

02/8/2014
our results suggest that TGF-beta cytokine family signaling through Smad3 protects neurons in the damaged cortex and hippocampus at early time points after injury.

Smad3 deficiency increases cortical and hippocampal neuronal loss following traumatic brain injury.
Villapol S, Wang Y, Adams M, Symes AJ.

02/1/2014
a nuclear envelope-localized mechanism of inactivating TGF-beta signaling in which MAN1 competes with transcription factors for binding to Smad2 and Smad3 and facilitates their dephosphorylation by PPM1A.

Inhibition of TGF-β signaling at the nuclear envelope: characterization of interactions between MAN1, Smad2 and Smad3, and PPM1A.
Bourgeois B, Gilquin B, Tellier-Lebègue C, Östlund C, Wu W, Pérez J, El Hage P, Lallemand F, Worman HJ, Zinn-Justin S., Free PMC Article

01/18/2014
Notch signaling can down-regulate TGF-beta1/Smad3-induced fibroblast-myofibroblast transition and that RLX could exert its well known anti-fibrotic action through the up-regulation of this pathway.

Relaxin prevents cardiac fibroblast-myofibroblast transition via notch-1-mediated inhibition of TGF-β/Smad3 signaling.
Sassoli C, Chellini F, Pini A, Tani A, Nistri S, Nosi D, Zecchi-Orlandini S, Bani D, Formigli L., Free PMC Article

01/4/2014
The Smad binding element is essential for Hoxd11/lacZ expression in transgenic mice

Direct activation of a mouse Hoxd11 axial expression enhancer by Gdf11/Smad signalling.
Gaunt SJ, George M, Paul YL.

12/21/2013
We propose that Smad2/3 and IRF4 cooperatively transactivate the Il9 promoter and play an important role in regulating allergic immune responses by inducing Th9 cells.

Smad2/3 and IRF4 play a cooperative role in IL-9-producing T cell induction.
Tamiya T, Ichiyama K, Kotani H, Fukaya T, Sekiya T, Shichita T, Honma K, Yui K, Matsuyama T, Nakao T, Fukuyama S, Inoue H, Nomura M, Yoshimura A.

11/16/2013
The activated Akt in turn interacts with Smad3, resulting in the inhibition of TGF-beta-induced Smad3 phosphorylation and consequently the reduction of p-Smad3 results in the decreased binding to the specific binding site of the foxp3 promoter.

TNF-α impairs differentiation and function of TGF-β-induced Treg cells in autoimmune diseases through Akt and Smad3 signaling pathway.
Zhang Q, Cui F, Fang L, Hong J, Zheng B, Zhang JZ.

11/16/2013
reduction in IGF-IR reduces p-Akt, allowing for dissociation and nuclear translocation of Smad3

Interactions between p-Akt and Smad3 in injured muscles initiate myogenesis or fibrogenesis.
Dong Y, Lakhia R, Thomas SS, Dong Y, Wang XH, Silva KA, Zhang L., Free PMC Article

10/19/2013
Smad3 binds Scleraxis and Mohawk and regulates tendon matrix organization.

Smad3 binds Scleraxis and Mohawk and regulates tendon matrix organization.
Berthet E, Chen C, Butcher K, Schneider RA, Alliston T, Amirtharajah M., Free PMC Article

09/28/2013
results indicate that down-regulation of Smad3 expression by siRNA can accelerate wound-healing; may inhibit wound contraction. siRNA-targeted inhibition of Smad3 may represent valuable therapeutic tool for palatal mucoperiosteal wound-healing.

Down-regulation of Smad3 accelerates palatal wound repair.
Yoneda N, Yasue A, Watanabe T, Tanaka E.

09/21/2013
these data provides the first evidence that 14-3-3 sigma is a Smad3-dependent target gene of TGF-beta1.

14-3-3 σ is a new target up-regulated by transforming growth factor-β1 through a Smad3-dependent mechanism.
Hong HY, Jeon WK, Kim SJ, Kim BC.

09/21/2013
Association of beta-catenin with P-Smad3 but not LEF-1 dissociates in vitro profibrotic from anti-inflammatory effects of TGF-beta1.

Association of β-catenin with P-Smad3 but not LEF-1 dissociates in vitro profibrotic from anti-inflammatory effects of TGF-β1.
Tian X, Zhang J, Tan TK, Lyons JG, Zhao H, Niu B, Lee SR, Tsatralis T, Zhao Y, Wang Y, Cao Q, Wang C, Wang Y, Lee VW, Kahn M, Zheng G, Harris DC.

09/14/2013
TGF-beta-Smad3 signaling may maintain T-cell tolerance by suppressing co-stimulation-dependent mobilization of anabolic pathways.

The TGF-β-Smad3 pathway inhibits CD28-dependent cell growth and proliferation of CD4 T cells.
Delisle JS, Giroux M, Boucher G, Landry JR, Hardy MP, Lemieux S, Jones RG, Wilhelm BT, Perreault C.

08/31/2013
Data indicate that mad2, smad3 and smad7 were all broadly expressed throughout the early embryonic pancreatic epithelium.

Smad signaling pathways regulate pancreatic endocrine development.
El-Gohary Y, Tulachan S, Guo P, Welsh C, Wiersch J, Prasadan K, Paredes J, Shiota C, Xiao X, Wada Y, Diaz M, Gittes G., Free PMC Article

07/27/2013
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