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Last update 08 May 2025

DVL1

Last update 08 May 2025

Basic Info

Synonyms

dishevelled segment polarity protein 1, Dishevelled-1, DSH homolog 1

+ [2]

Introduction

Participates in Wnt signaling by binding to the cytoplasmic C-terminus of frizzled family members and transducing the Wnt signal to down-stream effectors. Plays a role both in canonical and non-canonical Wnt signaling. Plays a role in the signal transduction pathways mediated by multiple Wnt genes. Required for LEF1 activation upon WNT1 and WNT3A signaling. DVL1 and PAK1 form a ternary complex with MUSK which is important for MUSK-dependent regulation of AChR clustering during the formation of the neuromuscular junction (NMJ).

Drugs associated with DVL1

RS4690

Target

DVL1

Mechanism

DVL1 inhibitors

Active Org.

Sapienza University of Rome

Originator Org.

Sapienza University of Rome

Active Indication

Colonic Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with DVL1

100 Translational Medicine associated with DVL1

0 Patents (Medical) associated with DVL1

318

Literatures (Medical) associated with DVL1

01 Mar 2025·Acta Histochemica

Spatiotemporal distribution of Wnt signaling pathway markers in human congenital anomalies of kidney and urinary tract

Article

Author: Kelam, Nela ; Perutina, Ilija ; Maglica, Mirko ; Filipović, Natalija ; Prusac, Ivana Kuzmić ; Vukojević, Katarina ; Ghahrani, Nasrollah ; Kablar, Boris ; Mišković, Josip ; Bošnjak, Marko ; Rizikalo, Azer ; Racetin, Anita

This study aimed to investigate the spatiotemporal expression patterns of key markers involved in regulating the canonical and non-canonical Wnt pathway during human fetal kidney development, comparing healthy (CTRL) and congenital anomalies of the kidney and urinary tract (CAKUT) affected kidneys. Human fetal kidneys, ranging from the 18th to the 38th developmental weeks, including various CAKUT phenotypes (horseshoe, dysplastic, duplex and hypoplastic), underwent double immunofluorescence microscopy analysis following antibody staining. Immunoreactivity levels were quantified in different kidney structures, and expression dynamics were assessed using linear and nonlinear regression modeling techniques. The study revealed a decrease in the overall protein expression of acetylated α-tubulin during normal kidney development, while the highest percentage of positive cells was observed in the horseshoe kidney (HK), thus disturbing microtubule composition in normal cell division and differentiation. Additionally, a continuous decrease of inversin-positive cells in hypoplastic (HYP) and duplex kidneys (UD), but the exponential growth of DVL-1 expression score in dysplastic kidneys (DYS) with developmental age, result in suppression of final kidney differentiation by continuous canonical Wnt signaling activation, thus supporting the essential role of the switch from canonical to non-canonical Wnt pathway in nephrogenesis. Furthermore β-catenin-positive cells in dysplastic and hypoplastic kidney exhibited the highest percentage of positive signal, with a decline in β-catenin positive cells over time in the control group, indicating disturbances in transition from canonical to non-canonical Wnt pathway in CAKUT-affected kidneys. The findings suggest that the crosstalk between canonical and non-canonical Wnt signaling pathways is crucial for normal nephrogenesis, highlighting their potential roles in normal and dysfunctional kidney development.

01 Jan 2025·Genes & Diseases

Naked cuticle homolog 2 controls the differentiation of osteoblasts and osteoclasts and ameliorates bone loss in ovariectomized mice

Article

Author: Shan, Liying ; Yang, Xiaoli ; Zhu, Endong ; Yuan, Hairui ; Li, Xiaoxia ; Liao, Xiaoxia ; Wang, Baoli ; Zhou, Jie

Naked cuticle homolog 2 (NKD2) has been recognized as an antagonist of Wnt/β-catenin signaling and a tumor suppressor. The role of NKD2 in osteoblast and osteoclast differentiation and the mechanism are not fully understood. In this study, we identified the up-regulation of NKD2 during osteoblast and adipocyte differentiation. Functional experiments revealed that NKD2 stimulated osteoblast differentiation and suppressed adipocyte formation. Furthermore, NKD2 down-regulated the expression of receptor activator of nuclear factor-κB ligand in bone marrow mesenchymal stem cells and inhibited osteoclast formation from osteoclast precursor cells. Mechanistic investigations revealed that the regulation of osteoblast and adipocyte differentiation by NKD2 involved Wnt/β-catenin and tuberous sclerosis complex subunit 1 (TSC1)/mechanistic target of rapamycin complex 1 (mTORC1) signaling pathways. Unlike in undifferentiated mesenchymal cells where NKD2 promoted Dishevelled-1 degradation, in the cells differentiating toward osteoblasts or adipocytes NKD2 down-regulated secreted frizzled related protein 1/4 expression and failed to destabilize Dishevelled-1, thereby activating Wnt/β-catenin signaling. Moreover, NKD2 bound to TSC1 and inhibited mTORC1 signaling. Further investigation uncovered an interplay between TSC1/mTORC1 and Wnt/β-catenin signaling pathways. Finally, transplantation of NKD2-overexpressing bone marrow mesenchymal stem cells into the marrow of mice increased osteoblasts, reduced osteoclasts and marrow fat, and partially prevented bone loss in ovariectomized mice. This study provides evidence that NKD2 in mesenchymal stem/progenitor cells reciprocally regulates the differentiation of osteoblasts and adipocytes by modulating Wnt/β-catenin and mTORC1 pathways and inhibits osteoclast formation by down-regulating receptor activator of nuclear factor-κB ligand. It suggests that NKD2 up-regulation may ameliorate postmenopausal bone loss.

01 Nov 2024·Archives of Biochemistry and Biophysics

The LncRNA6524/miR-92a-2-5p/Dvl1/Wnt/β-catenin axis promotes renal fibrosis in the UUO mouse model

Article

Author: Qiu, Shuangfa ; Zhang, Guoxiu ; Xie, Yuxin ; Zhang, Dongshan ; Pan, Jian

LncRNAs are reported to participate in multiple biological and pathological processes, including renal fibrosis due to obstructive nephropathy. However, the function and mechanisms of each lncRNA in this context differ. In this study, we created a fibrosis model in vitro using TGF-β1 treatment and in vivo through unilateral ureteral obstruction. We demonstrated that lncRNA6524 expression increased in both models, as confirmed by qPCR. Additionally, we discovered that lncRNA6524 mediates the TGF-β1-induced accumulation of extracellular matrix (ECM) proteins in BUMPT cells. We investigated the mechanism using dual luciferase reporter assays, immunofluorescence, and qPCR. Our results indicate that lncRNA6524 acts as a sponge for miR-92a-2-5p, promoting renal fibrosis by upregulating the Dvl1/Wnt/β-catenin signaling pathway. In summary, our findings demonstrate a linear regulatory relationship among lncRNA6524, miR-92a-2-5p, and the Dvl1/Wnt/β-catenin axis in renal epithelial cells during kidney obstruction. This highlights a new potential target for treating obstruction-related renal fibrosis.

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DVL1

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