Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
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. De plus, nous expédions SMAD5 Anticorps (111) et SMAD5 Protéines (14) et beaucoup plus de produits pour cette protéine.
Showing 4 out of 8 products:
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 (Montrer SMAD1 Kits ELISA)/5 and MAP kinase (Montrer MAPK1 Kits ELISA) signaling system (ERK (Montrer MAPK1 Kits ELISA) signalling) is essential for haemogenic endothelium-based haematopoietic stem cell emergence.
this study uncovers that smad1 (Montrer SMAD1 Kits ELISA) and smad9 (Montrer SMAD9 Kits ELISA) 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 (Montrer FGF10 Kits ELISA), tgfb2 (Montrer TGFB2 Kits ELISA), pax9 (Montrer PAX9 Kits ELISA), and smad5 revealed their necessity in zebrafish palatogenesis.
maternally supplied Smad5 is already required to mediate ventral specification prior to zygotic Bmp2 (Montrer BMP4 Kits ELISA)/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 (Montrer SMAD1 Kits ELISA) and Smad5.
Data show that Smad5 expression is ubiquitous during testis development but becomes cell-specific in the adult.
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 (Montrer SMAD1 Kits ELISA) pathway may be a novel target in addressing cognitive deficit of SZ in future studies.
the BMP-2 (Montrer BMP2 Kits ELISA)/Smad1 (Montrer GARS Kits ELISA)/5/RUNX2 (Montrer RUNX2 Kits ELISA) signaling pathway participates in the silicon-mediated induction of COL-1 and osteocalcin (Montrer BGLAP Kits ELISA) synth
miR (Montrer MLXIP Kits ELISA)-23a and miR (Montrer MLXIP Kits ELISA)-27a target SMAD5 and regulate apoptosis in human granulosa cells via the FasL (Montrer FASL Kits ELISA)-Fas (Montrer FAS Kits ELISA) pathway
Our findings suggest that suppression of miR (Montrer MLXIP Kits ELISA)-222-3p activity promoted osteogenic differentiation hBMSCs through regulating Smad5-RUNX2 (Montrer RUNX2 Kits ELISA) signaling axis.
Overexpression of the BMP4 (Montrer BMP4 Kits ELISA)/SMAD4 (Montrer SMAD4 Kits ELISA)/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 (Montrer L3MBTL1 Kits ELISA) 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 (Montrer AKT1 Kits ELISA) and SMAD1 (Montrer GARS Kits ELISA)/5 during long-period culture.
balance between Smad1 (Montrer GARS Kits ELISA)/5- and Smad2 (Montrer SMAD2 Kits ELISA)/3-dependent signaling defines the outcome of the effect of TGF-beta (Montrer TGFB1 Kits ELISA) on atherosclerosis where Smad1 (Montrer GARS Kits ELISA)/5 is responsible for proatherogenic effects
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 (Montrer CA8 Kits ELISA).
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 (Montrer SMAD4 Kits ELISA)/smad5 pathway.
Up-regulation of miR (Montrer MLXIP Kits ELISA)-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 (Montrer RUNX2 Kits ELISA)) expression through S1PR2 (Montrer S1PR2 Kits ELISA)/RhoA (Montrer RHOA Kits ELISA)/ROCK/Smad1 (Montrer SMAD1 Kits ELISA)/5/8 signaling.
We discovered that Smad1 (Montrer SMAD1 Kits ELISA)/5/4-Amhr2 (Montrer AMHR2 Kits ELISA)-cre KO females have malformed oviducts that subsequently develop oviductal diverticuli. In addition, uteri from Smad1 (Montrer SMAD1 Kits ELISA)/5/4-Amhr2 (Montrer AMHR2 Kits ELISA)-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 (Montrer TGFB1 Kits ELISA)-stimulated BMP R-Smad (Montrer SMAD1 Kits ELISA) signaling mechanism in interstitial cells of the developing lung.
Thyroid-specific Smad1 (Montrer SMAD1 Kits ELISA) and Smad5 double-knockout (Smad1 (Montrer SMAD1 Kits ELISA)/5(dKO)) mice displayed growth retardation, hypothyroidism and defective follicular architecture.
Smad1 (Montrer SMAD1 Kits ELISA) and Smad5 have overlapping functions to govern hepcidin (Montrer HAMP Kits ELISA) transcription. Moreover, erythropoietin (Montrer EPO Kits ELISA) and erythroferrone target Smad1 (Montrer SMAD1 Kits ELISA)/5 signaling and require Smad1 (Montrer SMAD1 Kits ELISA)/5 to suppress hepcidin (Montrer HAMP Kits ELISA) expression.
miR (Montrer MLXIP Kits ELISA)-106b-5p and miR-17-5p are novel Smad5 regulators.
BetA can enhance in vivo osteogenic potentials of BMP2 (Montrer BMP2 Kits ELISA), possibly via stimulating Smad 1 (Montrer SMAD1 Kits ELISA)/5/8 and p38 (Montrer CRK Kits ELISA) pathways, and combination of both agents can be considered as a therapeutic strategy for bone diseases.
Data show that in R-Smad (Montrer SMAD1 Kits ELISA) proteins Smad1 (Montrer SMAD1 Kits ELISA);Smad5 knockout embryonic stem cells (mESCs), the bone morphogenetic proteins (BMP)-SMAD (Montrer SMAD1 Kits ELISA) signaling is dispensable for self-renewal.
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).
a detailed computational model for TGF-beta (Montrer TGFB1 Kits ELISA) signalling that incorporates elements of previous models together with crosstalking between Smad1 (Montrer SMAD1 Kits ELISA)/5/8 and Smad2 (Montrer SMAD2 Kits ELISA)/3 channels through a negative feedback loop dependent on Smad7 (Montrer SMAD7 Kits ELISA).
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.
mothers against decapentaplegic homolog 5
, SMA- and MAD-related protein 5
, SMAD 5
, SMAD family member 5
, mothers against DPP homolog 5
, MAD, mothers against decapentaplegic homolog 5
, SMAD, mothers against DPP homolog 5
, mothers against decapentaplegic, drosophila, homolog of, 5
, MAD homolog 5
, Smad 5
, Mothers against decapentaplegic homolog 5