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. Low SMAD3 expression is associated with pre-eclampsia.

2. 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.

3. 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.

4. 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.

5. 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.

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

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

8. 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.

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

10. The data from the present study indicate that arapid increase in SMAD3 expression is crucial for osteogenesis and suggest a role for PDMCs in the treatment of patients with osteoporosis.

11. The current meta-analysis revealed that the G variant of SMAD3 rs12901499 polymorphism increased the risk of osteoarthritis in Caucasians [meta-analysis]

12. The increase in protein expression level of the ligand TGFbeta1 was 285 +/- 1.15% higher and its receptor TGFbetaRII was 170 +/- 0.98% higher in hippocampus of patients with Hippocampal Sclerosis (HS) in comparison to the autopsy hippocampal control samples. The expression of the downstream signalling molecules, SMAD3 is 157 +/- 0.13% and 106 +/- 0.17% higher in patients with HS as compared to both types of non-seizure...

13. SET9-deficient fibroblasts exhibit globally altered gene expression profiles in response to TGFB1, whilst overexpression of SET9 enhances SMAD3 transcriptional activity. SET9 facilitates nuclear import of SMAD3 and controls SMAD3 protein degradation via ubiquitylation.

14. The role of SMAD3 in the exosomes-mediated crosstalk between primary and circulating HCC cells.

15. PSPC1 increases transforming growth factor-beta1 (TGF-beta1) secretion through an interaction with phosphorylated and nuclear Smad2/3 to potentiate TGF-beta1 autocrine signaling, promoting epithelial mesenchymal transformation, stemness and metastasis.

16. The data show that TGFB1 induces THBS1 expression via Smad3 which contributes to the invasive behavior during glioblastoma multiforme expansion.

17. In the present study, we assessed whether smad family member 3 gene(SMAD3) rs12901499 polymorphism was associated with the risk of osteoarthritis by the meta-analysis

18. Report a group of locally recurrent superficial acral tumors, characterized by bland spindle cell fascicular growth, occasional zonation pattern, ERG positivity, and recurrent EWSR1-SMAD3 gene fusions.

19. ONECUT2 activates SMAD3, which regulates hypoxia signaling through modulating HIF1alpha chromatin-binding, leading neuroendocrine prostate cancers to exhibit higher degrees of hypoxia compared to prostate adenocarcinomas.

20. Authors propose that the pro-differentiation action of SMAD3 inhibits dedifferentiation that is required for HCASMC to expand and stabilize disease plaque as they respond to vascular stresses, counteracting the protective dedifferentiating activity of TCF21 and promoting disease risk.

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. 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

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

3. 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

4. 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.

5. 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.

6. 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.

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

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

9. 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.

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

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

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

13. We provide the evidence that over-expression of miR-145 could inhibit osteoclast differentiation, at least partially, by decreasing Smad3 expression

14. Activin signaling through SMAD2/3 in retinal progenitor cells regulates expression of transcription factors involved in cell type determination and promotes photoreceptor lineage specification.

15. conclude that VDD promotes tumor growth in the context of Smad3 disruption, potentially through regulation of TLR7 expression and beta-catenin activation

16. SMAD3 is regulated by miR-489 in pulmonary fibrosis.miR-489 suppresses fibroblast differentiation by targeting Smad3.

17. Alendronate (ALN)-augmented IL-1beta production and cell death require Smad3 and ASC activation, and SIS3 and anti-ASC antibodies may serve as palliative agents for necrotizing inflammatory diseases caused by ALN

18. CRP is pathogenic in type-2 diabetes (T2DN). CRP may promote CD32b- NF-kappaB signaling to mediate renal inflammation; whereas, CRP may enhance renal fibrosis in T2DN via CD32b-Smad3-mTOR signaling.

19. A Smad3-PTEN regulatory loop controls proliferation and apoptotic responses to TGF-beta in mouse endometrium.

20. These findings indicate that both systemic factors and intrinsic properties of skin cells contribute to enhanced wound healing and less inflammatory reaction observed in Smad3 knock-out mice.

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.