anti-SMAD3 (SMAD3) Antikörper

Zebrafish SMAD, Mothers Against DPP Homolog 3 (SMAD3) Interaktionspartner

1. Data suggest that Clock1a coordinates mesoderm development and primitive hematopoiesis in embryos by up-regulating Nodal-Smad3 signaling; Clock1a alterations produce embryonic defects with shortened body length, lack of ventral tail fin, or partial defect of the eyes; Clock1a activates Smad3a promoter via its E-box1 element. (Clock1a = clock circadian regulator a; Nodal = nodal modulator 1; Smad3a = SMAD family member 3a)

2. Smad3 is mainly active in post-mitotic, non-proliferating cells with a role in TGF-beta control of zebrafish spinal cord development

3. Nodal signaling and mesendoderm induction depend on Smad2/3 and suggest that transforming growth factor-beta signals other than Nodal also contribute to Smad2/3 signaling and embryonic patterning.

4. although the role of Smad proteins in mediating Nodal signaling is well-documented, the functional characterization of Ttrap provides insight into a novel Smad partner that plays an essential role in the fine-tuning of this signal transduction cascade

5. Smad2/3 activities play important roles not only in mesendodermal development but also in neural development during early vertebrate embryogenesis

Rabbit SMAD, Mothers Against DPP Homolog 3 (SMAD3) Interaktionspartner

1. Data indicate that cardiac contractility modulation (CCM) therapy exerted protective effects against myocardial fibrosis potentially by inhibiting TGF-beta1/Smad3 signaling pathway in chronic heart failure .

2. study suggested that TGF-beta1/Smad3/smad7 is a major pathway which plays an important role in the regulation of the IUA and specific inhibitor of Smad3 (SIS3) may provide a new therapeutic strategy for IUA.

Human SMAD, Mothers Against DPP Homolog 3 (SMAD3) Interaktionspartner

1. Transforming growth factor beta1 promotes fibroblast-like synoviocytes migration and invasion via TGF-beta1/Smad signaling in rheumatoid arthritis.

2. Dexamethasone may antagonize airway remodeling by regulating TGF-beta1/Smad3 signaling pathway, which likely to play a role in the treatment of bronchial asthma.

3. IL-37d is a functional cytokine that negatively regulates pro-inflammatory cytokines expression in a Smad3-dependent manner.

4. PIM1 could interact with Smad2 or Smad3 in the nucleus and subsequently phosphorylate Smad2 and Smad3 to induce the expression of transcription factors.

5. The strongest DNA methylation changes in atopic asthma were detected in the promoter region of SMAD3 gene at chr 15q22.33 and introns of DDO/METTL24 genes at 6q21.

6. Smad2 knockdown resulted in no inhibitory effect, whereas Smad3 knockdown completely suppressed TGF-beta-induced TF expression.

7. TGFbeta signaling can shift from inhibiting to promoting breast cancer development via HER2/EGFR AKT-mediated phosphorylation of Smad3 at S208, enhancing its nuclear accumulation and upregulation of EMT-related genes

8. Smad proteins SMAD2 and SMAD3 are core transcription factors involved in TGF-beta signaling, and they interact with cofactors to control the expression of TGF-beta-dependent genes.

9. Aortic Dimensions and Clinical Outcome in Patients With SMAD3 Mutations.

10. Case Reports: fibroblastic/myofibroblastic tumors with EWSR1-SMAD3 gene rearrangement.

11. Data indicate that PPAR-g agonists represent an attractive treatment tool and by suppression of cell growth (in vitro and ex vivo models) and of invasion via blockade of MAPK cascade and TGFb/SMADs signaling, respectively, and its role in cancer bioenergetics and metabolism indicate that PPAR-g agonists represent an attractive treatment tool for non small cell lung cancer .

12. Low SMAD3 expression is associated with pre-eclampsia.

13. our data point at SMYD3 as a pivotal SMAD3 cofactor that promotes TGFbeta-dependent mesenchymal gene expression and cell migration in breast cancer, and support SMYD3 as a promising pharmacological target for anti-cancer therapy.

14. Data showed that Pfn1 depletion is associated with SMAD3 upregulation in breast cancer cells (BCC). Although knockdown and overexpression experiments revealed that SMAD3 has an inhibitory effect on the outgrowth of breast cancer cells, SMAD3 knockdown alone was not sufficient to enhance the outgrowth potential of Pfn1-depleted BCC.

15. The interaction between miR-152-5p and Smad3 occurs through the Erk1/2 and Akt pathways and regulates collagen3 production. In summary, study demonstrates that miR-152-5p/Smad3 regulatory pathways involved in fibrotic progression may be a potential therapeutic target of keloids.

16. These findings identify SOX4 as an important SMAD3 co-factor controlling transcription of pro-metastatic genes and context-dependent shaping of the cellular response to TGF-b. Targeted disruption of the interaction between these factors may have the potential to disrupt pro-oncogenic TGF-b signaling, thereby impairing tumorigenesis.

17. Schizandrin conferred its beneficial effects possibly by downregulating Smad3 and inhibiting the activation of JNK and NF-kappaB pathways.

18. During iron deficiency, SMAD3 and SMAD4 expression was significantly decreased via proteasomal degradation, allowing for derepression of iron target genes.

19. The results revealed an innovative function of the miR-1254 in controlling SMAD3 and pro-fibrosing elements as well as the wound healing response in LX-2, attenuating the scaring repair of the injured tissue.

20. Expression of p-Smad3 was significantly upregulated in the temporal cortex of patients with temporal lobe epilepsy.

Xenopus laevis SMAD, Mothers Against DPP Homolog 3 (SMAD3) Interaktionspartner

1. E2a is necessary to drive transcription of Smad2/3 target genes, including critical regulators of dorsal cell fate and morphogenesis

Pig (Porcine) SMAD, Mothers Against DPP Homolog 3 (SMAD3) Interaktionspartner

1. TAZ confers SMAD3 sensitivity to the smooth muscle actin promoter.

2. HSP70 indirectly interacted with Smad3.

3. Activin A and overexpression of SMAD2/3 significantly promoted expressions of porcine NANOG and OCT4,maintaining induced pluripotent stem cell self-renewal through up-regulation of Nanog/OCT4 expression.

4. Smad3 regulate the activity and stability of myocardin-related transcription factor during epithelial-myofibroblast transition

5. SP1 and SMAD3 are required for high glucose-induced p21(WAF1) gene transcription in LLC-PK1 cells.

Mouse (Murine) SMAD, Mothers Against DPP Homolog 3 (SMAD3) Interaktionspartner

1. Mstn regulated Jmjd3 expression through SMAD2/SMAD3

2. These data demonstrated that paeonol could alleviate CCl4-induced liver fibrosis through suppression of hepatic stellate cells activation via inhibiting the TGF-beta/Smad3 signaling.

3. SMAD2 and SMAD3 were expressed in the nuclei of primordial granulosa cells but were mostly excluded in early growing follicles.

4. Extracellular matrix protein overexpression and Smad1 activation were observed in the glomeruli of db/db mice but were suppressed in the glomeruli of Smad3+/-; db/db mice. Smad3 activation enhanced the phosphorylation of Smad1 C-terminal domain but decreased the phosphorylation of linker domain, thus regulating Smad1 activation in advanced glycation end product-treated mesangial cells.

5. Skeletal muscle stem cells underwent a switch from beta-catenin-Lef1 to Smad3-Lef1 interactions during the postnatal switch from proliferation to quiescence, with beta-catenin-Lef1 interactions recurring during damage-induced reactivation.

6. serine 204 within Smad3 is the key Pin1-binding site during inhibition of myoblast fusion

7. our data suggest that RepSox regulates osteoclast differentiation, bone resorption, and OVX-induced OP via the suppression of the Smad3 and JNK/AP-1 pathways.

8. Depletion of Dicer and microRNAs may upregulate Smad2/3-related signaling pathway to enhance the progression of chronic kidney disease.

9. Genome-wide experiments demonstrate that the proneural factor ASCL1 assists SMAD3 in the binding to a subset of enhancers. Once located at the enhancers, SMAD3 recruits the histone demethylase JMJD3 and the remodeling factor CHD8, creating the appropriate chromatin landscape to allow enhancer transcription and posterior gene activation

10. miR-21 knockout exacerbated AngII-induced thoracic aortic dissecting aneurysm formation in mice, which was associated with TGF-beta/Smad3 signaling dysfunction.

11. Our findings generate a mouse model to study the roles of SMAD2/3 in the uterus and serve to provide insight into the mechanism by which the endometrium can escape the plethora of growth regulatory proteins

12. Here the authors have demonstrated that TGF-beta/Smad signaling plays an important role in Laser-induced choroidal neovascularization formation through down-regulation of VEGF and TNF-alpha expressions.

13. In healing myocardial infarction, myofibroblast- and cardiomyocyte-specific activation of Smad3 has contrasting functional outcomes that may involve activation of an integrin/reactive oxygen axis.

14. The application of the combined siRNAs of SPARC, CCR2, and SMAD3 genes ameliorated inflammation and fibrosis in bleomycin-induced mice. It systemically reinstated multiple biopathways, probably through controlling on different cell types including fibroblasts, monocytes/macrophages, endothelial cells and others.

15. Ash1l upregulates Smad3 expression by directly targeting Smad3 promoter to increase local H3K4 trimethylation.

16. Data indicate E4BP4/NFIL3 as a direct Smad3 target gene critical for NK cell differentiation.

17. Data suggest that Smad-specific E3 ubiquitin ligase 2 (SMURF2)-mediated SMAD3 protein (SMAD3) monoubiquitination interferes with the formation of a SMAD3-vitamin D receptor (VDR) complex.

18. These data indicate that SMAD3- and beta-catenin-dependent induction occurs in the taurine transporter knockout mouse

19. Cav-3 and Smad3 may be involved in the occurrence and development of viral myocarditis.

20. In pancreata of mice and rats, TGFB promotes peripheral nociceptive sensitization via a direct effect on primary sensory neurons mediated by intra-neuronal SMAD3.

Cow (Bovine) SMAD, Mothers Against DPP Homolog 3 (SMAD3) Interaktionspartner

1. Data show that the transcription factor Smad3 (Smad3) gene was expressed ubiquitously in 11 bovine tissues and displayed different expression patterns between muscle and adipose tissue.

2. the present work provides evidence supporting a functional role of SMAD2/3 in bovine early embryogenesis

3. Mechanical compression not only with physiological but also with excessive stress can activate Smad2/3P signaling, which is known to be protective for articular cartilage and to block chondrocyte terminal differentiation.

4. 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.