SMAD, Mothers Against DPP Homolog 5 (SMAD5) ELISA Kits

Human SMAD, Mothers Against DPP Homolog 5 (SMAD5) Interaktionspartner

1. Here, the authors show that TGF-beta-induced SMAD1/5 phosphorylation requires members of two classes of type I receptor, TGFBR1 and ACVR1, and establish a new paradigm for receptor activation where TGFBR1 phosphorylates and activates ACVR1, which phosphorylates SMAD1/5.

2. these results suggested that miR-21 be mechanistically implicated in the regulation of osteogenic differentiation of hPDLSCs by targeting Smad5.

3. Memory T cells targeting oncogenic mutations in KRAS, SMAD5, and MUC4 detected in peripheral blood of colon cancer patients have been isolated.

4. We demonstrated high expression of miR-145 associated with late stage and unfavorable prognosis of esophageal cancer. We identified SMAD5 as direct target of miR-145, the suppressed expression of which consequently led to increased cell proliferation and migration/invasion.

5. Smad5 acts as a intracellular pH messenger and maintains the bioenergetic homeostasis of cells by regulating cytoplasmic metabolic machinery.

6. Differential expression of TGF-beta superfamily members and role of Smad1/5/9-signalling in chondral versus endochondral chondrocyte differentiation.

7. Data suggest that differences in expression levels in granulosa-like tumor cells and granulosa cells (GCs) from patients with polycystic ovary syndrome (PCOS) are due to increased expression of microRNA-27a-3p in GCs caused by insulin resistance in PCOS; microRNA-27a-3 expression is up-regulated in GCs in PCOS; overexpression of miR-27a-3p inhibits SMAD5 expression and promotes apoptosis. (SMAD5 = SMAD family member 5)

8. Here the involvement of the pathway in adult brain function is suggested. This exploratory study establishes a strategy to better identify neuronal molecular signatures that are potentially associated with mental illness and cognitive deficits. We propose that the SMAD pathway may be a novel target in addressing cognitive deficit of SZ in future studies.

9. the BMP-2/Smad1/5/RUNX2 signaling pathway participates in the silicon-mediated induction of COL-1 and osteocalcin synth

10. miR-23a and miR-27a target SMAD5 and regulate apoptosis in human granulosa cells via the FasL-Fas pathway

11. Our findings suggest that suppression of miR-222-3p activity promoted osteogenic differentiation hBMSCs through regulating Smad5-RUNX2 signaling axis.

12. Overexpression of the BMP4/SMAD4/SMAD5 signaling pathway could predict poor clinical outcome in skull base chordomas, suggesting activation of this pathway is involved in chordoma pathogenesis.

13. The polycomb group protein L3MBTL1 represses a SMAD5-mediated hematopoietic transcriptional program in human pluripotent stem cells.

14. adult human Sertoli cells assumed similar morphological features, stable global gene expression profiles and numerous proteins, and activation of AKT and SMAD1/5 during long-period culture.

15. balance between Smad1/5- and Smad2/3-dependent signaling defines the outcome of the effect of TGF-beta on atherosclerosis where Smad1/5 is responsible for proatherogenic effects

16. among the 15 SNPs, rs3206634 was significantly associated with KD in a recessive model (odds ratio = 2.31, p = 0.019), whereas there was no association between any of the 15 SNPs and CALs.

17. Our results indicated that KGN promoted the type-I collagen synthesis of dermal fibroblasts in vitro and in the dermis of mice through activation of the smad4/smad5 pathway.

18. Inhibiting Smurf1 mediated ubiquitination of Smad1/5.

19. Specific gene siRNAs knock-down further confirmed the osteogenic effects of Genistein on BMP2, SMAD5 and RUNX2 protein expression

20. Results indicate that BMP/Smad signaling pathway was altered during the period of osteogenesis, and that the activities of p-Smad1/5 were required for Saos-2 cells viability and differentiation induced by fluoride.

Zebrafish SMAD, Mothers Against DPP Homolog 5 (SMAD5) Interaktionspartner

1. TGFbeta1a regulates zebrafish posterior lateral line formation via Smad5 mediated pathway.

2. Alk3 and Alk3b, as well as SMAD5, are essential cellular mediators of BMP signaling in zebrfish.

3. Data show that interplay of Smad1/5 and MAP kinase signaling system (ERK signalling) is essential for haemogenic endothelium-based haematopoietic stem cell emergence.

4. this study uncovers that smad1 and smad9 act redundantly to each other downstream of smad5 to mediate ventral specification and to regulate embryonic myelopoiesis.

5. Functional investigation of a subset of these genes, fgf10a, tgfb2, pax9, and smad5 revealed their necessity in zebrafish palatogenesis.

6. maternally supplied Smad5 is already required to mediate ventral specification prior to zygotic Bmp2/7 signaling to establish the initial dorsoventral asymmetry

7. Data show that patterning of the eye primordia in Smad5-deficient embryos starts during blastula and early gastrula stages.

8. that specificity of BMP signaling output, with respect to hematopoiesis, can be explained by differential functions of Smad1 and Smad5.

9. Data show that Smad5 expression is ubiquitous during testis development but becomes cell-specific in the adult.

Cow (Bovine) SMAD, Mothers Against DPP Homolog 5 (SMAD5) Interaktionspartner

1. 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.

Mouse (Murine) SMAD, Mothers Against DPP Homolog 5 (SMAD5) Interaktionspartner

1. The luciferase reporter assay confirmed a direct interaction between miR-132-3p and Smad5. Thus, miR-132-3p maybe regulates osteoblast differentiation via Smad5 in response to cyclic tensile stress.

2. SMAD1/5 signaling in osteoclasts regulates bone formation via coupling factors.

3. SMAD5 is crucial for expanding amniotic ectoderm rapidly into a stretchable squamous sheet to accommodate exocoelom expansion, axial growth and folding morphogenesis.

4. CD137 signaling is a new regulator of angiogenesis by modulating the Smad1/5-NFATc1 pathway.

5. miR-155 inhibited osteoblast differentiation by downregulating the translation of SMAD5 in mouse preosteoblast cells. Inhibition of miR-155 promoted osteogenic potential and thus it can be used as a potential target in the treatment of bone defects.

6. Up-regulation of miR-93 may contribute to the progression of morphine tolerance by targeting Smad5 in mouse model of bone cancer pain

7. Sphingosine 1 phosphate also up-regulated runt-related transcription factor 2 (Runx2) expression through S1PR2/RhoA/ROCK/Smad1/5/8 signaling.

8. We discovered that Smad1/5/4-Amhr2-cre KO females have malformed oviducts that subsequently develop oviductal diverticuli. In addition, uteri from Smad1/5/4-Amhr2-cre KO females exhibit multiple defects in stroma, epithelium, and smooth muscle layers and fail to assemble a closed uterine lumen upon embryo implantation, with defective uterine decidualization that led to pregnancy loss at early to mid-gestation.

9. these studies characterize an accessory TGF-beta-stimulated BMP R-Smad signaling mechanism in interstitial cells of the developing lung.

10. Thyroid-specific Smad1 and Smad5 double-knockout (Smad1/5(dKO)) mice displayed growth retardation, hypothyroidism and defective follicular architecture.

11. Smad1 and Smad5 have overlapping functions to govern hepcidin transcription. Moreover, erythropoietin and erythroferrone target Smad1/5 signaling and require Smad1/5 to suppress hepcidin expression.

12. miR-106b-5p and miR-17-5p are novel Smad5 regulators.

13. BetA can enhance in vivo osteogenic potentials of BMP2, possibly via stimulating Smad 1/5/8 and p38 pathways, and combination of both agents can be considered as a therapeutic strategy for bone diseases.

14. Data show that in R-Smad proteins Smad1;Smad5 knockout embryonic stem cells (mESCs), the bone morphogenetic proteins (BMP)-SMAD signaling is dispensable for self-renewal.

15. Data show that R-Smad Proteins SMAD1 and SMAD5, which transduce bone morphogenetic protein (BMP) signals, recognize enhancer regions together with Kruppel-like factors KLF4 and KLF5 in naive embryonic stem cell (mESCs).

16. The crystal structure of Smad5-MH1 domain in complex with a composite DNA sequence demonstrates that the MH1 domain is targeted to a binding site with modular binding modes, and the length of the DNA spacer affects the MH1 assembly.

17. The findings demonstrate for the first time that KMUP-1 can promote osteoblast maturation and differentiation in vitro via BMP-2/Smad1/5/8 and Wnt/beta-catenin pathways.

18. FLI1 and GATA2 are upstream regulators of SMAD1 and SMAD5 expression in endothelial cells.

19. Data indicate that PDGF-AA promotes mesenchymal stem cel migration via bone morphogenetic protein 2 (BMP2)-smad proteins smad1/5/8 activation requires lysosome-mediated degradation of PDGF alpha Receptor (PDGFRalpha).

20. some pSMAD1/5 targets, like Gata3, function specifically in transit amplifying cell lineage-progression.