Ignet

Gene Information

Gene symbol: WNT3A

Gene name: wingless-type MMTV integration site family, member 3A

HGNC ID: 15983

Related Genes

#	Gene Symbol	Number of hits
1	BMP2	1 hits
2	BMP4	1 hits
3	CTNNB1	1 hits
4	DKK1	1 hits
5	FGF4	1 hits
6	GSK3B	1 hits
7	JUP	1 hits
8	MSX2	1 hits
9	SHH	1 hits
10	TNF	1 hits
11	VEGFA	1 hits
12	WNT2	1 hits
13	WNT7A	1 hits

Related Sentences

#	PMID	Sentence
1	15507471	The proinvasive activity of Wnt-2 is mediated through a noncanonical Wnt pathway coupled to GSK-3beta and c-Jun/AP-1 signaling.
2	15507471	Here, we show that two activators of the canonical Wnt/beta-catenin transcription pathway, namely Dvl-2, the Axin 501-560 fragment binding glycogen synthase kinase -3beta (GSK-3beta), and the negative Wnt regulator wt-Axin did not alter cell invasion into type I collagen.
3	15507471	In addition, both Dvl-2 and Axin 501-560 exerted a permissive action on the proinvasive activity of HGF and intestinal trefoil factor.
4	15507471	Upstream activation of Wnt signaling by the Wnt-2 and Wnt-3a ligands, stable overexpression of Wnt-2, as well as GSK-3beta inhibition by lithium, SB216763, and GSK-3beta dominant negative forms (K85R and R96E) conferred the invasive phenotype through several proinvasive pathways.
5	15507471	Induction of the matrix metalloprotease MMP-7 (matrilysin) gene and protein by Wnt-2 was abolished by inactivation of the AP-1 binding site in the promoter.
6	15507471	Accordingly, invasion induced by Wnt-2 was prevented by soluble FRP-3 and FRP-1, sequestration of Gbetagamma subunits, depletion of the GSK-3beta protein by RNA interference, the c-Jun dominant negative mutant TAM67 and was not reversed by wt-Axin.
7	15507471	Thus, the proinvasive activity of Wnt-2 is mediated by a noncanonical Wnt pathway using GSK-3beta and the AP-1 oncogene.
8	17109623	Here we describe a modified in vitro procedure to direct differentiation of three clonal hESC lines, hES 3.1, hES 3.2 and hES 3.3 efficiently to spinal motor neurons by using various differentiation factors namely retinoic acid (RA), sonic hedgehog (Shh), bone morphogenetic protein-2 (BMP-2) and Wnt3A.
9	17982705	Regulation of in vitro vascular calcification by BMP4, VEGF and Wnt3a.
10	17982705	In addition, these factors render VSMCs responsive to BMP4 and Wnt3a ligands.
11	17982705	Neither BMP-4 nor Wnt3a could induce mineralization in short-term (up to 8 days) cultures of primary mouse VSMCs.
12	17982705	In addition, expression profiling suggests a novel role in vascular calcification for the matrix proteins previously known to regulate bone formation and mineralization (including MMP3, fibulin, 11betahydroxysteroid dehydrogenase 1 and retinoic acid receptor responder 2).
13	17982705	Regulation of in vitro vascular calcification by BMP4, VEGF and Wnt3a.
14	17982705	In addition, these factors render VSMCs responsive to BMP4 and Wnt3a ligands.
15	17982705	Neither BMP-4 nor Wnt3a could induce mineralization in short-term (up to 8 days) cultures of primary mouse VSMCs.
16	17982705	In addition, expression profiling suggests a novel role in vascular calcification for the matrix proteins previously known to regulate bone formation and mineralization (including MMP3, fibulin, 11betahydroxysteroid dehydrogenase 1 and retinoic acid receptor responder 2).
17	17982705	Regulation of in vitro vascular calcification by BMP4, VEGF and Wnt3a.
18	17982705	In addition, these factors render VSMCs responsive to BMP4 and Wnt3a ligands.
19	17982705	Neither BMP-4 nor Wnt3a could induce mineralization in short-term (up to 8 days) cultures of primary mouse VSMCs.
20	17982705	In addition, expression profiling suggests a novel role in vascular calcification for the matrix proteins previously known to regulate bone formation and mineralization (including MMP3, fibulin, 11betahydroxysteroid dehydrogenase 1 and retinoic acid receptor responder 2).
21	18433704	TNF-alpha induces the osteogenic bone morphogenetic protein-2 (BMP-2), Msx2, Wnt3a, and Wnt7a mRNAs and leads to increased aortic calcium accumulation.
22	18433704	Treatment with the TNF-alpha neutralizing antibody infliximab abrogates aortic BMP-2-Msx2-Wnt3a and Wnt7a signaling and attenuates aortic calcium accumulation significantly.
23	18433704	Mice with vascular TNF-alpha augmented by the SM22-TNF-alpha transgene upregulate the aortic Msx2-Wnt3a/Wnt7a axis.
24	20019166	Wnt/beta-catenin signaling mediates renal fibrosis in several model systems including diabetic nephropathy.
25	20019166	Dickkopf-1 (DKK-1) is an endogenous inhibitor of Wnt/beta-catenin signaling, but whether DKK-1 modulates diabetic nephropathy is unknown.
26	20019166	In vitro, HG increased expression of DKK1, receptor Kremen-2, TGF-beta1, and fibronectin in mesangial cells.
27	20019166	Loss and gain of DKK1 function modulated HG-mediated c-Jun, TGF-beta1, and fibronectin expression.
28	20019166	DKK1 mediated HG-induced phosphorylation of Ser45-beta-catenin and reduction of nuclear beta-catenin levels, but not phosphorylation of ERK kinase.
29	20019166	Wnt3a protein and the beta-catenin (Delta45) mutation increased nuclear beta-catenin but abrogated HG-induced DKK1 and fibronectin expression.
30	20019166	Taken together, DKK1 mediates HG-induced destabilization of beta-catenin and matrix accumulation in mesangial cells.
31	20179324	Activation of canonical wingless-type MMTV integration site family (Wnt) signaling in mature adipocytes increases beta-catenin levels and leads to cell dedifferentiation and insulin resistance.
32	20179324	Typical adipogenic markers were reduced while undifferentiated cell markers like Pref-1/Dlk1, Wnt10b, and Gata2 were increased.
33	20179324	Wnt3a stabilized beta-catenin in the absence of the LRP6 receptor and with maintained axin and Dickkopf-1 protein expression.
34	20179324	PPARgamma was repressed and PPARgamma ligands could not restore the adipogenic markers or reduce the beta-catenin levels.
35	20179324	These results identify a novel pathway in mature adipose cells that is critical for maintaining the normal adipocyte phenotype and insulin sensitivity.
36	21151107	Using this culture system as a model to study human intestinal development, we identified that the combined activity of WNT3A and FGF4 is required for hindgut specification whereas FGF4 alone is sufficient to promote hindgut morphogenesis.