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Human Polyclonal SMAD1 Primary Antibody für WB - ABIN1881815
Ye, Yu, Hu, Lu, Xie: Alterations of dendritic cell subsets in the peripheral circulation of patients with cervical carcinoma. in Journal of experimental & clinical cancer research : CR 2010
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Human Polyclonal SMAD1 Primary Antibody für WB - ABIN3042628
Tao, Hu, Li, Liu, Wu, Li, Fu, Wei, Luo: Tranilast prevents the progression of chronic cyclosporine nephrotoxicity through regulation of transforming growth factor ?/Smad pathways. in Transplantation proceedings 2011
Show all 3 Pubmed References
Human Monoclonal SMAD1 Primary Antibody für IF, IHC (p) - ABIN517610
Nakajima, Yanagihara, Nishii: Temporal and regional patterns of Smad activation in the rat hippocampus following global ischemia. in Journal of the neurological sciences 2014
Human Polyclonal SMAD1 Primary Antibody für WB - ABIN967044
Zhu, Kavsak, Abdollah, Wrana, Thomsen: A SMAD ubiquitin ligase targets the BMP pathway and affects embryonic pattern formation. in Nature 1999
Human Polyclonal SMAD1 Primary Antibody für WB - ABIN362414
Yamaguchi, Zhu, Yu, Sasaki, Umetsu, Kidachi, Ryoyama et al.: Serum-free mouse embryo cells generate a self-sustaining feedback loop for an astrocyte marker protein and respond to cytokines and bisphenol A in accordance with the subtle difference in their ... in Cell biology international 2007
Data show that interplay of Smad1/5 and MAP kinase (zeige MAPK1 Antikörper) signaling system (ERK (zeige MAPK1 Antikörper) signalling) is essential for haemogenic endothelium-based haematopoietic stem cell emergence.
this study uncovers that smad1 and smad9 (zeige SMAD9 Antikörper) act redundantly to each other downstream of smad5 (zeige SMAD5 Antikörper) to mediate ventral specification and to regulate embryonic myelopoiesis.
that specificity of BMP signaling output, with respect to hematopoiesis, can be explained by differential functions of Smad1 and Smad5 (zeige SMAD5 Antikörper).
This report provides a genetic analysis of primary nociceptive neuron mechanisms that promote sensitization in response to injury. Drosophila melanogaster larvae whose primary nociceptive neurons were reduced in levels of specific components of the BMP signaling pathway, were injured and then tested for nocifensive responses to a normally subnoxious stimulus.
LTR sequence of the MDG4 (zeige MOD(MDG4) Antikörper) retrotransposon contains the MAD protein (zeige MXD1 Antikörper) binding site that affects the east-dependent repression
we identify key roles for the Zelda and Zerknullt transcription factors in establishing the resulting expression domain, and find widespread binding of insulator proteins to the Mad and Brinker-bound genomic regions. Analysis of embryos lacking the BEAF-32 insulator protein shows reduced transcription of a peak BMP target gene and a reduction in the number of amnioserosa cells, the fate specified by peak BMP signaling.
Mad linker phosphorylations control the intensity and range of the BMP-activity gradient in developing Drosophila tissues.
During development, synaptic pMad accumulation followed the arrival and clustering of ionotropic glutamate (zeige GRIN2A Antikörper) receptors at neuromuscular junction synapses.
The actions of Brat at synapses are mediated through mothers against decapentaplegic (Mad), the signal transduction effector of the bone morphogenetic protein (BMP) signaling pathway.
Mad has distinct signal transduction roles in the BMP (zeige TGFb Antikörper) and Wnt (zeige WNT4 Antikörper) pathways depending on its phosphorylation state.
Yorkie (zeige YAP1 Antikörper) and Mad physically bind each other, and 410 bp minimal enhancer of bantam that responds to Yorkie:Mad in vivo and in cultured cells, was identified.
Heterodimers of SAX and TKV play an important role in extending the BMP activity gradient by facilitating DPP diffusion and assisting GBB signaling through functional complexes with type II receptors.
importin-beta11 function interacts with the bone morphogenic protein (zeige TGFb Antikörper) pathway to regulate a pool of phosphorylated mothers against decapentaplegic that must be present at the presynapse for its proper development and function
Data show that miR (zeige MLXIP Antikörper)-26b-5p suppresses Twist1 (zeige TWIST1 Antikörper)-induced EMT (zeige ITK Antikörper), invasion, and metastasis of HCC (zeige FAM126A Antikörper) cells by targeting SMAD1 (zeige GARS Antikörper).
Testosterone promoted tube formation of human umbilical endothelial cells, which was blocked by c-Src (zeige SRC Antikörper) and ERK1/2 (zeige MAPK1/3 Antikörper) inhibitors or by the knockdown of Smad1 (zeige GARS Antikörper).
Low doses of IL1B (zeige IL1B Antikörper) activate the BMP/Smad signaling pathway to promote the osteogenesis of periodontal ligament stem cells, but higher doses of IL1B (zeige IL1B Antikörper) inhibit BMP/Smad signaling through the activation of NF-kappaB (zeige NFKB1 Antikörper) and MAPK (zeige MAPK1 Antikörper) signaling, inhibiting osteogenesis.
Store operated calcium entry negatively regulates the Smad1 (zeige GARS Antikörper) signaling pathway and inhibits Col (zeige HDAC1 Antikörper) IV protein production in glomerular mesangial cells.
A significant association was found between the low expression of inhibitory protein SMAD-7 (zeige SMAD7 Antikörper) and both zeta-chain-associated protein kinase (zeige CDK7 Antikörper) 70-negative cells (p = 0.04) and lower apoptotic index (p = 0.004). No differences were observed in SMAD-2 (zeige SMAD2 Antikörper)/3 expression. In conclusion, our results demonstrate a significant correlation between greater SMAD-1 (zeige GARS Antikörper)/8 and lower SMAD-4 (zeige SMAD4 Antikörper) expression in chronic lymphocytic leukemia cells
melatonin treatment was found to downregulate TNFalpha (zeige TNF Antikörper)-induced SMURF1 (zeige SMURF1 Antikörper) expression and then decrease SMURF1 (zeige SMURF1 Antikörper)-mediated ubiquitination and degradation of SMAD1 (zeige GARS Antikörper) protein
The expression of specific targets Smad1 (zeige GARS Antikörper) and Osterix (zeige SP7 Antikörper) was significantly increased in the presence of Pi and restored by coincubation with Mg(2 (zeige MUC7 Antikörper)+). As miR (zeige MLXIP Antikörper)-30b, miR (zeige MLXIP Antikörper)-133a, and miR (zeige MLXIP Antikörper)-143 are negatively regulated by Pi and restored by Mg(2 (zeige MUC7 Antikörper)+) with a congruent modulation of their known targets Runx2 (zeige RUNX2 Antikörper), Smad1 (zeige GARS Antikörper), and Osterix (zeige SP7 Antikörper), our results provide a potential mechanistic explanation of the observed upregulation of these master switches of o
the BMP-2 (zeige BMP2 Antikörper)/Smad1 (zeige GARS Antikörper)/5/RUNX2 (zeige RUNX2 Antikörper) signaling pathway participates in the silicon-mediated induction of COL-1 and osteocalcin (zeige BGLAP Antikörper) synth
Regulation of impaired angiogenesis in diabetic dermal wound healing by microRNA-26a is mediated by the increased expression of its target gene, SMAD1 (zeige GARS Antikörper).
The expression SMAD1 (zeige GARS Antikörper) protein showed a significant correlation with lung cancer differentiation and lymphatic metastasis (P < 0.05), but not with genders, ages, tumor sizes and histological types of lung cancer patients (P>0.05).
AA-enhanced cardiomyogenesis thus relies on the ability of AA to modulate the ratio of SMAD signaling among the TGFbeta (zeige TGFB1 Antikörper)-superfamily receptor signaling pathways
Sphingosine 1 phosphate also up-regulated runt-related transcription factor 2 (Runx2 (zeige RUNX2 Antikörper)) expression through S1PR2 (zeige S1PR2 Antikörper)/RhoA (zeige RHOA Antikörper)/ROCK/Smad1/5/8 signaling.
these results identify the PI3K-GSK3 (zeige GSK3b Antikörper)-SMAD1 axis as a central node integrating multiple signaling networks that govern bone formation and homeostasis.
We discovered that Smad1/5/4-Amhr2 (zeige AMHR2 Antikörper)-cre KO females have malformed oviducts that subsequently develop oviductal diverticuli. In addition, uteri from Smad1/5/4-Amhr2 (zeige AMHR2 Antikörper)-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 (zeige TGFB1 Antikörper)-stimulated BMP R-Smad signaling mechanism in interstitial cells of the developing lung.
these results identify a novel function of YAP (zeige YAP1 Antikörper) in neocortical astrocytic differentiation and proliferation, and reveal a BMP2 (zeige BMP2 Antikörper)-YAP (zeige YAP1 Antikörper)-SMAD1 pathway underlying astrocytic differentiation in the developing mouse neocortex.
Dynamin (zeige DNM1 Antikörper)-dependent endocytosis of Bone Morphogenetic Protein2 (BMP2 (zeige BMP2 Antikörper)) and its receptors is dispensable for the initiation of Smad signaling
Thyroid-specific Smad1 and Smad5 (zeige SMAD5 Antikörper) double-knockout (Smad1/5(dKO)) mice displayed growth retardation, hypothyroidism and defective follicular architecture.
Smad1 and Smad5 (zeige SMAD5 Antikörper) have overlapping functions to govern hepcidin (zeige HAMP Antikörper) transcription. Moreover, erythropoietin (zeige EPO Antikörper) and erythroferrone target Smad1/5 signaling and require Smad1/5 to suppress hepcidin (zeige HAMP Antikörper) expression.
Actin cytoskeleton depolymerization inhibites BMP2 (zeige BMP2 Antikörper) signaling via blocking of Smad by dephosphorylated CNN1 (zeige CNN1 Antikörper) in osteoblast cells under simulated microgravity.
interactions between miR (zeige MYLIP Antikörper)-26 and the Smad1 3'UTR (zeige UTS2R Antikörper) modulate Smad1 function in the establishment of axial patterning.
a detailed computational model for TGF-beta (zeige TGFB1 Antikörper) signalling that incorporates elements of previous models together with crosstalking between Smad1/5/8 and Smad2 (zeige SMAD2 Antikörper)/3 channels through a negative feedback loop dependent on Smad7 (zeige SMAD7 Antikörper).
The protein encoded by this gene belongs to the SMAD, a family of proteins similar to the gene products of the Drosophila gene 'mothers against decapentaplegic' (Mad) and the C. elegans gene Sma. SMAD proteins are signal transducers and transcriptional modulators that mediate multiple signaling pathways. This protein mediates the signals of the bone morphogenetic proteins (BMPs), which are involved in a range of biological activities including cell growth, apoptosis, morphogenesis, development and immune responses. In response to BMP ligands, this protein can be phosphorylated and activated by the BMP receptor kinase. The phosphorylated form of this protein forms a complex with SMAD4, which is important for its function in the transcription regulation. This protein is a target for SMAD-specific E3 ubiquitin ligases, such as SMURF1 and SMURF2, and undergoes ubiquitination and proteasome-mediated degradation. Alternatively spliced transcript variants encoding the same protein have been observed.
MAD homolog 1
, SMAD, mothers against DPP homolog 1
, mothers against decapentaplegic homolog 1
, mothers against decapentaplegic-like protein 1
, MAD (mothers against decapentaplegic, Drosophila) homolog 1
, SMA- and MAD-related protein 1
, SMAD 1
, SMAD family member 1
, mothers against DPP homolog 1
, mother against decapentaplegic
, mothers against decapentaplegi
, mothers against decapentaplegic
, mothers against dpp
, phosphorylated smad
, MAD, mothers against decapentaplegic homolog 1
, Mad-related protein 1
, TGF-beta signaling protein 1
, transforming growth factor-beta signaling protein 1
, transforming growth factor-beta-signaling protein 1
, Smad 1
, mad-related protein 1
, mothers-against-DPP-related 1
, MAD homolog1 (mothers against decapentaplegic, Drosophila)
, mothers against DPP
, BMP pathway effector
, BMP signal transducer Smad1
, Sma- and Mad-related protein 1