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Regulates Wnt proteins sorting and secretion in a feedback regulatory mechanism. Additionally we are shipping WLS Antibodies (15) and WLS Proteins (5) and many more products for this protein.
we identified novel associations in WLS , ARHGAP1 (show ARHGAP1 ELISA Kits) , and 5' of MEF2C (show MEF2C ELISA Kits) ( P- values < 8x10 - 5 ; false discovery rate (FDR) q-values < 0.01) that were much more strongly associated with BMD (show BEST1 ELISA Kits) compared to the GWAS SNPs.
Our data suggest that Wls protein is related to tumor metastasis and advanced TNM (show ODZ1 ELISA Kits) stage, and may be used as a new marker for prognosis of gastric carcinoma.
These results indicate that WLS may play a role in invasion and metastasis of colorectal carcinoma.
Dysfunction of Wntless triggers the retrograde Golgi-to-ER transport of Wingless and induces ER stress.
Genetic variation at the WLS and CCDC170 (show CCDC170 ELISA Kits)/ESR1 (show ESR1 ELISA Kits) loci were found to be significantly associated with bone mineral density
This study has revealed a strong association between the expression of WLS and HER2 (show ERBB2 ELISA Kits) that has important biological and clinical implications.
This study identified CMTM8 (show CMTM8 ELISA Kits) as a new candidate tumor suppressor gene and GPR177 as a new candidate oncogene (show RAB1A ELISA Kits) in osteosarcoma.
GPR177 played an essential role in disease relapse and poor survival in patients with B-cell precursor acute lymphoblastic leukemia.
endogenous WLS binds Wnts in the endoplasmic reticulum, cycles to the plasma membrane, and then returns to the endoplasmic reticulum through the Golgi.
Colorectal tumors express elevated levels of Wnt3 and GPR177.
Wntless-deficient macrophages presented a unique subset of M2-like macrophages with anti-inflammatory, reparative, and angiogenic properties. Serial echocardiography studies revealed that mice lacking macrophage Wnt (show WNT2 ELISA Kits) secretion showed improved function and less remodeling 30 days after myocardial infarction.
GPR177 in Sertoli cells had no apparent influence on spermatogenesis, whereas loss of GPR177 in germ cells disrupted spermatogenesis in an age-dependent manner.
these results suggest that Gpr177 controls epithelial initiation of the fungiform placode through signaling via epithelial Wnt (show WNT2 ELISA Kits) ligands.
regulates chondrogenesis and osteogenesis through both canonical and noncanonical Wnt (show WNT2 ELISA Kits) signaling
Ablation of Wntless in endosteal niches impairs lymphopoiesis rather than hematopoietic stem cells maintenance.
Wls-mediated secretion of Wnt (show WNT2 ELISA Kits) ligands from the developing ventral body wall mesenchyme plays a critical role in fusion of the sternum and closure of the secondary body wall.
eletion of the Wls gene in odontoblasts appears to reduce canonical Wnt (show WNT2 ELISA Kits) activity, leading to inhibition of odontoblast maturation and root elongation.
The existence of spatial compartmentation in the rhombic lip and the interplay between Wls, Math1 (show ATOH1 ELISA Kits), and Pax6 (show PAX6 ELISA Kits) in the rhombic lip provides novel views of early cerebellar development.
Retromer dependent recycling of the Wnt secretion factor Wls is dispensable for stem cell maintenance in the mammalian intestinal epithelium
The loss of Wls in the ventral epithelium, which blocks the secretion of Wnt (show WNT2 ELISA Kits) proteins, resulted in dysgenesis of ventral musculature and genitourinary tract during embryonic development.
the chaperon Wls and its ligands Wnt9a (show WNT9A ELISA Kits) and Wnt5b (show WNT5B ELISA Kits) are expressed in the ectoderm, whereas juxtaposed chondrocytes express Frzb (show FRZB ELISA Kits) and Gpc4 (show GPC4 ELISA Kits).
disruption of wls resulted in a significant loss of craniofacial bone, whereas lack of gpc4 (show GPC4 ELISA Kits), wnt5b (show WNT5B ELISA Kits) and wnt9a (show WNT9A ELISA Kits) resulted in severely delayed endochondral ossification.
Homozygous wls mutants show a reduction in two cell populations that contribute to the presumptive dorsal habenulae.
The relatively ubiquitous expression of GPR177 suggests that this protein may serve to regulate Wnt (show WNT2 ELISA Kits) secretion in a variety of embryonic and adult tissue types.
The uncharacterized Drosophila protein Evi5 was identified as an essential membrane trafficking regulator, and the molecular mechanism by which Evi5 regulates BC migration was described.
Syx1A, Rab11, and its effector Myosin5 were required for proper Evi vesicle release.
DSNX3 regulates Wg secretion via retromer-dependent Wls recycling
Por-mediated lipidation of the S239-equivalent residue is essential for the interaction with, and secretion by, Wls.
we propose that Wntless represents an ancient partner for Wnts dedicated to promoting their secretion into the extracellular milieu.
The function of Srt is restricted to events occurring within the Wg-producing cells, study shows that srt is not required for any aspect of Hedgehog (Hh) signal transduction, suggesting specificity of srt for the Wg pathway.
Recent studies have identified Wntless (Wls) and the retromer complex as essential components involved in Wnt signaling.
Wg, clathrin-mediated endocytosis and retromer sustain a Wls traffic loop from the Golgi to the plasma membrane and back to the Golgi, thereby enabling Wls to direct Wnt (show WNT4 ELISA Kits) secretion.
WntD, a recently characterized Drosophila Wnt family member, does not require Porcupine or Wntless/Evi/Sprinter for its secretion or signaling activity
Regulates Wnt proteins sorting and secretion in a feedback regulatory mechanism. This reciprocal interaction plays a key role in the regulation of expression, subcellular location, binding and organelle-specific association of Wnt proteins. Plays also an important role in establishment of the anterior-posterior body axis formation during development (By similarity).
G protein-coupled receptor 177
, integral membrane protein GPR177
, protein evenness interrupted homolog
, protein wntless homolog
, putative NF-kappa-B-activating protein 373
, putative NFkB activating protein 373
, evenness interrupted