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anti-Mouse (Murine) WNT3A Antikörper:
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Human Polyclonal WNT3A Primary Antibody für IF (p), IHC (p) - ABIN733178
Gao, Yang, Gao, Xu, Niu, Li, Wen: Salvianolic acid B improves bone marrow-derived mesenchymal stem cell differentiation into alveolar epithelial cells type I via Wnt signaling. in Molecular medicine reports 2015
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Monoclonal WNT3A Primary Antibody für ELISA, WB - ABIN533801
Smolich, McMahon, McMahon, Papkoff: Wnt family proteins are secreted and associated with the cell surface. in Molecular biology of the cell 1994
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Human Polyclonal WNT3A Primary Antibody für IHC (p), ELISA - ABIN2477144
Skalská: [Use of linear logistic regression in classification of observations]. in Sborník v?deckých prací Léka?ské fakulty Karlovy univerzity v Hradci Králové. Supplementum 1991
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Human Polyclonal WNT3A Primary Antibody für ELISA, WB - ABIN2477145
Lai, Cheng, Cheng, Feasel, Beste, Peng, Nusrat, Moreno: SOX4 interacts with plakoglobin in a Wnt3a-dependent manner in prostate cancer cells. in BMC cell biology 2011
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Cow (Bovine) Polyclonal WNT3A Primary Antibody für IHC, WB - ABIN2787841
Chiquet, Blanton, Burt, Ma, Stal, Mulliken, Hecht: Variation in WNT genes is associated with non-syndromic cleft lip with or without cleft palate. in Human molecular genetics 2008
Human Monoclonal WNT3A Primary Antibody für ELISA, ICC - ABIN449669
Denysenko, Annovazzi, Cassoni, Melcarne, Mellai, Schiffer: WNT/β-catenin Signaling Pathway and Downstream Modulators in Low- and High-grade Glioma. in Cancer genomics & proteomics 2015
Results suggest that the miR-140-3p is involved in osteoblast differentiation as a critical regulatory factor between Wnt3a and TGFbeta3 signaling pathways.
These results indicate that the hepatocytic expression of TGF-beta and CTGF is mediated by Wnt signalling in Schistosoma japonicum infection.
This work provides a new link between Wnt3a and macrophage-mediated angiogenesis under glucose and oxygen deprivation in vitro.
Wnt signaling regulates airway epithelial stem cells in adult murine submucosal glands.
Lrp6 is the key mediator of Wnt3a signaling in osteoblasts and Lrp5 played a less significant role in mediating Wnt3a signaling.
These data define the mechanism responsible for the repressive effects of nitric oxide (NO) on the transcriptional activity of beta-catenin and link eNOS-derived NO to the modulation by VEGF of Wnt/beta-catenin-induced endothelial cell proliferation.
These results indicate that PEDF counters Wnt signaling to allow for osteoblast differentiation and provides a mechanistic insight into how the PEDF null state results in OI type VI.
These results suggest novel mechanisms for Wnt3a-induced osteoblast proliferation and cell survival via Npnt gene expression
this study shows that the Wnt3a expression levels in dendritic cells influences the generation of memory T cells after 5 days in co-culture with naive T cells through activation of the Wnt canonical pathway
Wnt3a induces Osx expression via p38 MAPK signaling in dental follicle cells. Wnt3a-induced Osx expression was inhibited in the presence of p38 mitogen-activated protein kinase (MAPK) inhibitors (SB203580 and SB202190) at gene and protein levels, as assessed by real-time PCR and immunocytohistochemistry, respectively.
Furthermore, pigment epithelium-derived factor (PEDF), a secreted glycoprotein known for its anti-tumor properties, blocked Wnt3a-directed induction of autophagy proteins. Autophagy inhibition was complemented by reciprocal regulation of the oxidative stress enzymes, superoxide dismutase 2 (SOD2) and catalase.
Ginkgo biloba exocarp extract inhibits tumor angiogenesis, which may be closely relevant to its effect in blockage of Wnt /beta-catenin-VEGF signaling pathway in Lewis lung carcinoma.
Western blot analysis demonstrated that following BMP2 and BMP7 cotransfection of MC3T3E1 cells, the protein expression levels of BMP2, BMP4, BMP6, BMP7, BMP9 and Wnt3a were increased compared with control cells
Wnt3a promotes macrophage-mediated bacterial killing by elevating CRAMP and BD1 levels.
Wnt3a acutely reduces nuclear acetyl-CoA, the necessary substrate for histone acetyltransferases, resulting in a global decrease in histone acetylation.
Wnt3a rapidly activated the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) pathway and pharmacological stimulation of cAMP/PKA signaling suppressed osteoclast differentiation
Mesenchymal Stem Cells Within Gelatin/CaSO4 Scaffolds Treated Ex Vivo with Low Doses of BMP-2 and Wnt3a Increase Bone Regeneration.
Wnt3a increased the expression of NeuroD1 and Ins2 in the hypothalamus.
that activation of the Wnt pathway made cells more readily tolerate ROS-caused mitochondria injury and cell apoptosis
Pin1 is indispensable for Wnt3a-induced osteoblast differentiation.
The miR-766-3p suppressed hepatocellular carcinoma (HCC) cell growth and invasion via a Wnt3a/PRC1 positive regulatory loop, and miR-766-3p may serve as a potential therapeutic target in HCC.
High WNT3A expression is associated with colon cancer proliferation and metastasis.
Wnt3A regulates the expression of 1,136 genes, of which 662 are upregulated and 474 are downregulated in CCD-18Co cells. A set of genes encoding inhibitors of the Wnt/beta-catenin pathway stand out among those induced by Wnt3A, which suggests that there is a feedback inhibitory mechanism.
we detected two potential associations with well-recognized skin cancer risk traits that modify miRNA-mRNA interactions: rs2325814 in the 3'UTR of the MLPH gene and rs752107 in the 3'UTR of the WNT3A gene.
PCR and western blot results showed that inhibiting the secretion of Wnt3A blocked the Wnt signaling pathway and prevented Nrf2 signaling. Notably, the Wnt inhibitor may serve as a radiosensitizing drug
Study found that Wnt3a highly expressed in hepatocellular carcinoma (HCC) tissues, and confirmed that Wnt3a plays an essential role in HCC progression. Activation of the Wnt3a pathway is accompanied by higher expression of Notch3. Furthermore, Wnt3a may be critical for HCC cell cycle and metastasis by regulating cell cycle regulatory proteins and the MAPK pathway.
WNT3A supports early stages such as the ALP activity, but it does neither improve later stages of the osteogenic differentiation nor it inhibits the genuine adipogenic differentiation of adipose tissue derived mesenchymal stem cells.
SP5 negatively regulates WNT3a transcriptional programs in human pluripotent stem cells.
Suggest that GPC5 is able to suppress the lung adenocarcinoma metastasis by competitively binding to Wnt3a and inactivating the Wnt/beta-catenin signaling pathway.
WNT3A/beta-catenin signaling inhibition is involved in leflunomide-mediated cytotoxic effects on renal carcinoma cells
BRG1 may contribute to colon cancer progression through upregulating WNT3A expression.
Here we describe a one-step immobilization technique to covalently bind WNT3A proteins as a basal surface with easy storage and long-lasting activity. We show that this platform is able to maintain adult and embryonic stem cells while also being adaptable for 3D systems
study reveals that Foxi1/miR-491-5p/Wnt3a/beta-catenin signaling is critical in the progression of GC. Targeting the pathway described in this study may open up new prospects to restrict the progression of gastric cancer
CHIR suppressed the hypertrophic propensity of the MSC-derived cartilage after in vivo implantation to an extent approaching that of WNT3A protein. These results indicate that CHIR may be a promising alternative for WNT3A protein for certain applications of human bone marrow-derived MSCs.
PEGylated Wnt3A liposomes associated with skeletal stem cell populations in human bone marrow and promoted osteogenesis.
The AChE plays a role in osteoblastic differentiation and is regulated by both Wnt3a and Runx2.
In promoting the self-renewal symmetric division of hTERT(high) prostate cancer cells, WNT3a dramatically decreased the ratio of hTERT(high) prostate cancer cells undergoing asymmetric division. Increased WNT/beta-catenin signal activation was also detected in hTERT(high) prostate cancer cells. hTERT-mediated CSC properties were at least partially dependent on beta-catenin.
the results indicate neighboring structural elements within full-length Wnt3a affect saposin-like subdomain (SLD) conformational stability. Moreover, SLD function(s) in Wnt proteins appear to have evolved away from those commonly attributed to SAPLIP family members.
Data suggest that PORCN exhibits substrate specificity that includes a Wnt3a peptide fragment (residues 199-219, with disulfide bonds); recombinant PORCN containing a point mutation (R228C) associated with focal dermal hypoplasia exhibits impaired acylation activity toward Wnt3a peptide fragment. (PORCN = porcupine O-acyltransferase; Wnt3a = Wnt family member 3A)
CPE through its N'-terminal sequence, forms aggregates with Wnt3a and possible endoplasmic reticulum (ER) stress leading to its loss of function.
Data suggest that Wnt3, Wnt3a, and Wnt8a bind to their respective receptors (Fz8, Lrp6, and Lypd6) in ordered plasma membrane environments; ordered plasma membrane environments appear to be essential for binding of Wnt proteins to their receptor complexes and stimulation of downstream signaling activity.
It was shown that Wnt3a-Wnt8a/beta-catenin signaling directly regulates ciliogenic transcription factor foxj1a expression and ciliogenesis in zebrafish Kupffer's vesicle.
In zebrafish embryos lacking Wnt3a, Wnt1 and Wnt10b, the expression of engrailed orthologs, pax2a and fgf8 is not maintained after mid-somitogenesis
data suggest a specific role for Wnt3a in the development of cardiac NCCs; propose that this function of wnt3a in r6 is partially mediated by crip2 expression in the premigratory cardiac NCCs, which subsequently affects cardiac function and PA patterning
Sulf1 does not affect Wnt3a-mediated activation of canonical Wnt signaling.
Wnt3a protein alone is sufficient to rescue the severe loss of inner ear structures resulting from dorsal but not ventral half ablations.
hindbrain-repressive Wnt3a/Meis3/Tsh1 circuit promotes neuronal differentiation and coordinates tissue maturation
Wnt3a thus acts downstream of FAK to balance anterior-posterior cell fate specification in the developing neural plate
Data suggest a new model for neural anteroposterior patterning, in which Wnt3a from the paraxial mesoderm induces posterior cell fates via direct activation of a crucial transcription factor in the overlying neural plate.
Wnt3A secretion from tectal cells along with ephrin-B1 signaling are specifically responsible for enhanced neural responses in the developing optic tectum.
The WNT gene family consists of structurally related genes which encode secreted signaling proteins. These proteins have been implicated in oncogenesis and in several developmental processes, including regulation of cell fate and patterning during embryogenesis. This gene is a member of the WNT gene family. It encodes a protein which shows 96% amino acid identity to mouse Wnt3A protein, and 84% to human WNT3 protein, another WNT gene product. This gene is clustered with WNT14 gene, another family member, in chromosome 1q42 region.
wingless-type MMTV integration site family, member 3A
, protein Wnt-3a-like
, protein Wnt-3a
, vestigial tail
, wingless-type MMTV integration site family, member 3 like
, wnt3 like
, wingless-type MMTV integration site family, member 3
, Wnt-3a homolog
, Wnt3a variant 3
, wingless-type MMTV integration site family member 3a
, wingless-related MMTV integration site 3A