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Human WNT5A Protein expressed in Wheat germ - ABIN1325364
Bazhin, Tambor, Dikov, Philippov, Schadendorf, Eichmüller: cGMP-phosphodiesterase 6, transducin and Wnt5a/Frizzled-2-signaling control cGMP and Ca(2+) homeostasis in melanoma cells. in Cellular and molecular life sciences : CMLS 2010
Results show that WNT5A induces castration resistance in prostate cancer (CRPC) cells and suggest that WNT5A may be a key gene that induces CRPC in the bone niche by recruiting and regulating macrophages through CCL2 and BMP6, respectively.
overexpression of Wnt5a in UM-UC-3 cells significantly increased cell viability, while knock-down of Wnt5a by its siRNA in SW780 cells dramatically sensitized cells to gemcitabine. Our results identified Wnt5a as a target gene of miR-129-5p.
miR-16-2* is negative correlated with bone formation and downregulated during osteogenic differentiation. WNT5A is a direct target gene of miR-16-2*.
Study shows that Wnt5a is associated with right ventricular dysfunction and adverse outcome in dilated cardiomyopathy (DCM) patients and may promote the progression of DCM through NFAT signaling.
Impaired Wnt5a signaling is associated with poor placentation and subsequent development of preeclampsia.
Decreased hepatic Wnt5a signaling is associated with hepatocellular carcinoma progression and poor prognosis.
Annotation of rs11918967 in WNT5A in tissues might be related to obesity.
Wnt5a expression is critical for proliferation of RL and VZ progenitors and Purkinje cell dendritogenesis during early embryonic development resulting in retarded development of cerebellum during postnatal stages.
Study shows that Wnt5a is upregulated in invasive glioblastoma tissues, and demonstrates that it may regulate the invasion of glioblastoma cells, at least in part via the Daam1/RhoA signaling pathway.
The findings suggest that Wnt5a expression may be involved in the inhibition of cell differentiation and the induction of an inflammatory response.
High WNT5A expression is associated with gliomas
Wnt5a promotes epithelial-to-mesenchymal transition and metastasis in non-small-cell lung cancer, which is involved in the activation of beta-catenin-dependent canonical Wnt signaling.
This study suggests that methylation of Wnt pathway genes, in addition to known CpG island methylator phenotype markers, may help predict treatment outcome and survival in patients with CRC[colorectal cancer.
non-canonical Wnt5a signalling could play a role in early human trophoblast development by promoting cell proliferation and survival.
These findings suggest that WNT-5A modulates fundamental mechanisms that affect airway smooth muscle contraction and thus may be of relevance for airway hyperresponsiveness in asthma.
We performed immunohistochemistry for Ki67, p16INK4a, and WNT5A in human HPs ( hyperplastic polyps), sessile serrated adenomas/polyps (SSA/Ps), and traditional serrated adenomas (TSAs) .The distribution of Ki67 and p16INK4a positive cells in TSAs was different from that in HPs and SSA/Ps.
Wnt5a-Ror2 signaling enhanced tongue SCC cell aggressiveness and promoted production of MMP-2 following DeltaNp63beta-mediated EMT
Here, the authors define WNT5A, a non-canonical Wnt ligand implicated in epithelial differentiation, repair, and cancer, as a direct transcriptional target that is activated by KLF4 in squamous epithelial cells.
These findings support that Wnt5a-Ror2 signaling plays a role in UC, support the potential use of Wnt5a as a prognostic marker and provide evidence that Wnt5a signaling may be used as an effective molecular target for novel therapeutic tools.
We show that rosiglitazone increases klotho and decreases Wnt5A in tumor cells, reducing the burden of both BRAF inhibitor-sensitive and BRAF inhibitor-resistant tumors in aged, but not young mice. However, when used in combination with PLX4720, tumor burden was reduced in both young and aged mice, even in resistant tumors
In midgastrula embryos, Wnt5a, Wnt11, and Wnt11b, but not Wnt3a, acted across many cell diameters to orient Prickle3/Vangl2 complexes away from their sources regardless of their positions relative to the body axis.
Xenopus adult stem cells originate from the larval absorptive cells expressing Ror2, which require Wnt5a/Ror2 signaling for their dedifferentiation accompanied by changes in cell morphology.
Data show that PAPC signaling via RhoA and Wnt5a/Ror2 activity are required to keep cells aligned in apical-basal orientation during invagination of the ear placode.
Data show that Rspo3 binds syndecan 4 and that together they activate Wnt5a/PCP signaling.
In an examination of signaling pathways in developing Xenopus lung, wnt5a was expressed in the mesenchyme layer of the entire lungs through stages 39-41.
Wnt5a reduces cell surface levels and promotes ubiquitination and degradation of SDC4 in dorsal mesodermal cells from Xenopus gastrulae.
Transcriptional regulation of XPAPC by XWnt-5A requires the receptor tyrosine kinase Ror2.
Xwnt-5a plays an instructive role in larval tail regeneration via Wnt/JNK signaling
WNT5A is a negative regulator of FSH-stimulated granulosa cell steroidogenesis in cattle.
There is an important role of Wnt5a in kidney development. Disrupted Wnt5a results in kidney cysts in zebrafish and pleiotropic abnormal kidney development in mice.
Wnt5a acts as a chemoattractant in the emerging limb bud where it contributes to the establishment of cell polarity that is likely to underlie the oriented cell behaviours
Identification of ISL1 transcriptional targets via ChIP-Seq and expression analyses revealed that Isl1 regulates several important signaling pathways during embryonic genital development, including the BMP, WNT, and FGF cascades.
Study shows that the interplay between CYR61-CTGF-NOV1 (CCN1) and Wnt5a in endothelial cells and pericytes determines the angiogenic outcome in a model of ischemic retinopathy. Data highlight the significance of CCN1-EC and CCN1-pericyte communication signals in driving physiological and pathological angiogenesis.
Activating effect of WNT5A regulated bone formation in response to hindlimb unloading in mice, and pretreatment with WNT5A partly rescued the osteoporosis caused by mechanical unloading.
The results of this study indicated that Shh, Sfrp1, and Wnt5a collaborate to direct the pathfinding of descending 5-HT axons in the brainstem.
calcineurin is a key regulator of Wnt5a-induced AQP2 activation without affecting intracellular cAMP level and PKA activity.
The findings demonstrate that induction of Vangl protein phosphorylation plays an essential role in transducing Wnt5a signaling to establish Planar cell polarity (PCP) in mammalian development, suggesting a phosphorylation-regulated "Vangl activity gradient" model in addition to the well-documented "Fz activity gradient" model in Wnt/PCP signaling.
Post-mitotic filopodial "pathfinding" is guided by mesenchymal WNT5A. Without WNT5A, some cells fail to tether basally and undergo apoptosis, leading to a shortened midgut.
We demonstrate with genetic evidence that the Wnt5a gradient acts as a global cue that is instructive in establishing planar cell polarity (PCP) in the limb mesenchyme, and that Wnt5a also plays a permissive role to allow Fgf4 and Fgf8 signaling to orient PCP.
Butyrate and bioactive proteolytic form of Wnt-5a regulate colonic epithelial proliferation and spatial development.
These data suggest that Wnt5a modulates the development of arthritis by promoting inflammation and osteoclast fusion, and provide the first mouse genetic evidence of a role for endogenous Wnt5a in autoimmune disease.
Here, we show that deletion of a single Wnt family member, Wnt5a, is sufficient to elicit profound disruptions in synaptic plasticity, structural maintenance, and learning and memory in adult mice, identifying the importance of this particular noncanonical Wnt in later-life functions.
Wnt5a promotes IL-6 and TIMP-1 release from mouse cardiac fibroblasts.
bivalent histone codes during odontogenic differentiation
WNT5A promoted spermatogonial stem cells activity both in vitro and in vivo.
results indicate that Wnt5a signaling restricts infection by antimony drug-sensitive and -resistant Leishmania donovani strains, at least in part by prohibiting parasite niche formation within host macrophages
During mouse embryonic stem cell (ESC) in vitro osteogenesis, the noncanonical WNT5a is expressed early on.
This study shows that Wnt5a is not required for development of the renal medulla and that loss of the renal medullary region in the Wnt5a-deleted kidney is caused by an abnormal ureter-bladder connection.
WNT5A in the bone marrow niche is required to regenerate hematopoietic stem cells and leukemic cells with functional ability to rearrange the actin cytoskeleton and engraft successfully.
This study describes the localization and functional role of WNT-5A in human and mouse fibrotic livers. Hepatic WNT-5A expression parallels collagen type I expression. In vivo and in vitro, the myofibroblasts were identified as the key hepatic cells producing WNT-5A. WNT-5A is under control of TGF-beta and its activities are primarily profibrotic.
we confirmed the requirement of Wnt5a in the deferoxamine-mediated osteoblast-promoting effects by analyzing the matrix mineralization of Wnt5a-deficient cells. The promoting effect of deferoxamine on matrix mineralization in wild-type cells was completely abolished in Wnt5a(-/-) cells.
Wnt-5A may be associated with cartilage destruction by promoting the expression of matrix metalloproteinases.
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 encodes a member of the WNT family that signals through both the canonical and non-canonical WNT pathways. This protein is a ligand for the seven transmembrane receptor frizzled-5 and the tyrosine kinase orphan receptor 2. This protein plays an essential role in regulating developmental pathways during embryogenesis. This protein may also play a role in oncogenesis. Mutations in this gene are the cause of autosomal dominant Robinow syndrome. Alternate splicing results in multiple transcript variants.
, protein Wnt-5a
, Wnt-5a protein
, wingless-related MMTV integration site 5A
, wingless-type MMTV integration site 5A
, wingless-type MMTV integration site family, member 5A
, protein Wnt-5a-like
, cell signaling molecule Wnt-5