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The protein encoded by SMAD5 is involved in the TGF-beta signaling pathway that results in an inhibition of the proliferation of hematopoietic progenitor cells. Additionally we are shipping SMAD5 Antibodies (125) and SMAD5 Proteins (14) and many more products for this protein.
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Smad5 acts as a intracellular pH messenger and maintains the bioenergetic homeostasis of cells by regulating cytoplasmic metabolic machinery.
Differential expression of TGF-beta (show TGFB1 ELISA Kits) superfamily members and role of Smad1 (show GARS ELISA Kits)/5/9-signalling in chondral versus endochondral chondrocyte differentiation.
Data suggest that differences in expression levels in granulosa-like tumor cells and granulosa cells (GCs (show GCLC ELISA Kits)) from patients with polycystic ovary syndrome (PCOS) are due to increased expression of microRNA-27a-3p in GCs (show GCLC ELISA Kits) caused by insulin (show INS ELISA Kits) resistance in PCOS; microRNA-27a-3 expression is up-regulated in GCs (show GCLC ELISA Kits) in PCOS; overexpression of miR (show MLXIP ELISA Kits)-27a-3p inhibits SMAD5 expression and promotes apoptosis. (SMAD5 = SMAD family member 5)
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 (show SMAD1 ELISA Kits) pathway may be a novel target in addressing cognitive deficit of SZ in future studies.
the BMP-2 (show BMP2 ELISA Kits)/Smad1 (show GARS ELISA Kits)/5/RUNX2 (show RUNX2 ELISA Kits) signaling pathway participates in the silicon-mediated induction of COL-1 and osteocalcin (show BGLAP ELISA Kits) synth
miR (show MLXIP ELISA Kits)-23a and miR (show MLXIP ELISA Kits)-27a target SMAD5 and regulate apoptosis in human granulosa cells via the FasL (show FASL ELISA Kits)-Fas (show FAS ELISA Kits) pathway
Our findings suggest that suppression of miR (show MLXIP ELISA Kits)-222-3p activity promoted osteogenic differentiation hBMSCs through regulating Smad5-RUNX2 (show RUNX2 ELISA Kits) signaling axis.
Overexpression of the BMP4 (show BMP4 ELISA Kits)/SMAD4 (show SMAD4 ELISA Kits)/SMAD5 signaling pathway could predict poor clinical outcome in skull base chordomas, suggesting activation of this pathway is involved in chordoma pathogenesis.
The polycomb group protein L3MBTL1 represses a SMAD5-mediated hematopoietic transcriptional program in human pluripotent stem cells.
adult human Sertoli cells assumed similar morphological features, stable global gene expression profiles and numerous proteins, and activation of AKT (show AKT1 ELISA Kits) and SMAD1 (show GARS ELISA Kits)/5 during long-period culture.
TGFbeta1a regulates zebrafish posterior lateral line formation via Smad5 mediated pathway.
Alk3 and Alk3b, as well as SMAD5, are essential cellular mediators of BMP signaling in zebrfish.
Data show that interplay of Smad1 (show SMAD1 ELISA Kits)/5 and MAP kinase (show MAPK1 ELISA Kits) signaling system (ERK (show MAPK1 ELISA Kits) signalling) is essential for haemogenic endothelium-based haematopoietic stem cell emergence.
this study uncovers that smad1 (show SMAD1 ELISA Kits) and smad9 (show SMAD9 ELISA Kits) act redundantly to each other downstream of smad5 to mediate ventral specification and to regulate embryonic myelopoiesis.
Functional investigation of a subset of these genes, fgf10a (show FGF10 ELISA Kits), tgfb2 (show TGFB2 ELISA Kits), pax9 (show PAX9 ELISA Kits), and smad5 revealed their necessity in zebrafish palatogenesis.
maternally supplied Smad5 is already required to mediate ventral specification prior to zygotic Bmp2 (show BMP4 ELISA Kits)/7 signaling to establish the initial dorsoventral asymmetry
Data show that patterning of the eye primordia in Smad5-deficient embryos starts during blastula and early gastrula stages.
that specificity of BMP signaling output, with respect to hematopoiesis, can be explained by differential functions of Smad1 (show SMAD1 ELISA Kits) and Smad5.
Data show that Smad5 expression is ubiquitous during testis development but becomes cell-specific in the adult.
a detailed computational model for TGF-beta (show TGFB1 ELISA Kits) signalling that incorporates elements of previous models together with crosstalking between Smad1 (show SMAD1 ELISA Kits)/5/8 and Smad2 (show SMAD2 ELISA Kits)/3 channels through a negative feedback loop dependent on Smad7 (show SMAD7 ELISA Kits).
SMAD5 is crucial for expanding amniotic ectoderm rapidly into a stretchable squamous sheet to accommodate exocoelom expansion, axial growth and folding morphogenesis.
CD137 (show TNFRSF9 ELISA Kits) signaling is a new regulator of angiogenesis by modulating the Smad1 (show SMAD1 ELISA Kits)/5-NFATc1 (show NFATC1 ELISA Kits) pathway.
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.
Up-regulation of miR (show MLXIP ELISA Kits)-93 may contribute to the progression of morphine tolerance by targeting Smad5 in mouse model of bone cancer pain
Sphingosine 1 phosphate also up-regulated runt-related transcription factor 2 (Runx2 (show RUNX2 ELISA Kits)) expression through S1PR2 (show S1PR2 ELISA Kits)/RhoA (show RHOA ELISA Kits)/ROCK/Smad1 (show SMAD1 ELISA Kits)/5/8 signaling.
We discovered that Smad1 (show SMAD1 ELISA Kits)/5/4-Amhr2 (show AMHR2 ELISA Kits)-cre KO females have malformed oviducts that subsequently develop oviductal diverticuli. In addition, uteri from Smad1 (show SMAD1 ELISA Kits)/5/4-Amhr2 (show AMHR2 ELISA Kits)-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.
these studies characterize an accessory TGF-beta (show TGFB1 ELISA Kits)-stimulated BMP R-Smad (show SMAD1 ELISA Kits) signaling mechanism in interstitial cells of the developing lung.
Thyroid-specific Smad1 (show SMAD1 ELISA Kits) and Smad5 double-knockout (Smad1 (show SMAD1 ELISA Kits)/5(dKO)) mice displayed growth retardation, hypothyroidism and defective follicular architecture.
Smad1 (show SMAD1 ELISA Kits) and Smad5 have overlapping functions to govern hepcidin (show HAMP ELISA Kits) transcription. Moreover, erythropoietin (show EPO ELISA Kits) and erythroferrone target Smad1 (show SMAD1 ELISA Kits)/5 signaling and require Smad1 (show SMAD1 ELISA Kits)/5 to suppress hepcidin (show HAMP ELISA Kits) expression.
miR (show MLXIP ELISA Kits)-106b-5p and miR-17-5p are novel Smad5 regulators.
The protein encoded by this gene is involved in the TGF-beta signaling pathway that results in an inhibition of the proliferation of hematopoietic progenitor cells. The encoded protein is activated by BMP type 1 receptor kinase. Three transcript variants encoding the same protein have been found for this gene.
MAD, mothers against decapentaplegic homolog 5
, SMA- and MAD-related protein 5
, SMAD, mothers against DPP homolog 5
, mothers against decapentaplegic homolog 5
, mothers against decapentaplegic, drosophila, homolog of, 5
, MAD homolog 5
, SMAD 5
, mothers against DPP homolog 5
, SMAD family member 5
, Mothers against decapentaplegic homolog 5
, Smad 5