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Last update 08 May 2025

EPDR1

Last update 08 May 2025

Basic Info

Synonyms

EPDR, EPDR1, ependymin related 1

+ [5]

Introduction

Binds anionic lipids and gangliosides at acidic pH.

Drugs associated with EPDR1

HG-1259

Target

EPDR1

Mechanism

EPDR1 modulators

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Neoplasms [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with EPDR1

100 Translational Medicine associated with EPDR1

0 Patents (Medical) associated with EPDR1

134

Literatures (Medical) associated with EPDR1

01 Feb 2025·Journal of Alzheimer’s Disease

Analysis of the causal relationship between five chosen factors and early-onset Alzheimer's disease: A Mendelian randomization study

Article

Author: Lu, Chunxin ; Zhou, Jiechao

Background This study aims to explore the causal relationship between five selected factors— lysosome , migrasomes , macrophage , fibroblast , and endothelium cell —and early-onset Alzheimer's disease (EOAD) through related genes, providing clues for EOAD research. MethodsUsing genes related to the five selected factors as exposure variables and EOAD as the disease outcome, significant genes were screened through Mendelian randomization (MR) analysis using the inverse-variance weighted (IVW) method, based on the OpenGWAS database. The selected genes were intersected with genes related to the exposure factors to assess the causal relationships between the five factors and EOAD.Results MR analysis identified 13 genes in total. Six of these genes were protective factors for EOAD, with LYST being the most significant (OR = 0.4259, 95% CI: 0.2218–0.8178, p = 0.0103). Seven genes were risk factors for EOAD, with NCF4 being the most significant (OR = 2.7207, 95% CI: 1.0229–7.2362, p = 0.0449). A total of 1925 genes related to lysosome , migrasomes , macrophage , fibroblast , and endothelium cell were analyzed. After intersection, 10 lysosome-related genes (NCF4, VIPAS39, LYST, SORT1, ARSB, EPDR1, SYNGR1, ANXA11, PYGB, CLN5) and 3 endothelium cell -related genes (ADM, NFIB, NKTR) were found to have significant causal relationships with EOAD. Conclusions There are genes related to lysosome and endothelium cell that have significant relationships with EOAD, while no causal relationships were found between migrasomes , macrophage , fibroblast , and EOAD. This study provides an important basis for further EOAD research.

01 Feb 2025·The Journal of Hand Surgery

A Genome-Wide Association Study and Rare Variant Analysis for Dupuytren Disease in a North American Population

Article

Author: Grandizio, Louis C ; Haley, Jeremy S. ; Haley, Jeremy S ; Carey, David J. ; Grandizio, Louis C. ; Smelser, Diane T. ; Delma, Stephanie ; Smelser, Diane T ; Carey, David J ; Klena, Joel C ; Klena, Joel C.

PURPOSEAlthough European genome-wide association studies (GWAS) have aided in defining genetic associations in Dupuytren disease (DD), North American populations have been infrequently analyzed. Additionally, there are a paucity of rare variant analyses (RVA) for DD, which can help define both trait variability and risk for low-frequency variants. Our purpose was to perform a GWAS and RVA for DD using a North American database.METHODSThe study cohort (cases and controls) consisted of patients from our institutional MyCode Community Health Initiative, an unselected clinical cohort. A GWAS was performed controlling for age, sex and body mass index. For the RVA, sequence kernel association test analysis was performed on the most significant genes from the GWAS. Sequence kernel association test is a regression method to test associations between common and rare genetic variants in a defined region and a specific trait while adjusting for covariates.RESULTSA total of 1,123 DD cases and 130,822 controls were included. DD cases were significantly older, more likely to be male, and had higher body mass indices. The GWAS yielded variants in two genes with a statistically significant difference between cases and controls: WNT7B and EPDR1. WNT7B variants rs9330811 (odds ratio, 1.96; 95% confidence interval, 1.73-2.23) and rs10448585 (odds ratio, 1.68; 95% confidence interval, 1.44-1.96) were the top hits. Variant rs2122625 in EPDR1 also reached genome-wide significance. The RVA indicated that WNT7B, DUXA, LOXL1, CSMD2, and TACC2 were significantly associated with a diagnosis of DD.CONCLUSIONSIn our North American population, GWAS yielded variants in two genes that were significantly associated with DD (WNT7B and EPDR), which likely contribute to abnormal proliferation of fibroblasts. Five rare variants (WNT7B, DUXA, LOXL1, CSMD2, and TACC2) were also significantly associated with DD.CLINICAL RELEVANCEAs disease-modifying treatments are explored, these data add to a growing body of literature defining genetic variants in DD.

01 Dec 2024·Journal of Biochemical and Molecular Toxicology

Genetic Interaction Between F‐Box Encoding UCC1 and RRM3 Regulates Growth Rate, Cell Size, and Stress Tolerance in Saccharomyces cerevisiae

Article

Author: Bairwa, Narendra K. ; Pandita, Monika ; Shoket, Heena ; Kumar, Rakesh

ABSTRACTUcc1, an F‐box motif‐containing protein of Saccharomyces cerevisiae encoded by UCC1 regulates energy metabolism through proteasomal degradation of citrate synthase Cit2 and inactivation of the glyoxylate cycle when glucose is present as the main carbon source in the growth medium. Rrm3, a Pif1 family DNA helicase, encoded by RRM3 regulates the movement of the replication forks during the DNA replication process. Here in this study, we present evidence of binary genetic interaction between both the genes, UCC1 and RRM3, that determine the growth rate, cell morphology, cell size, apoptosis, and stress response. The absence of both genes UCC1 and RRM3 leads to altered cell morphology, increased growth rate, utilization of alternate carbon sources, resistance to hydrogen peroxide, and susceptibility to acetic acid‐induced apoptosis. Further, the genetic interaction network analysis shows both the genes UCC1 and RRM3 interaction through the SGS1 and cross‐link among metabolic, glyoxylate, DNA replication, and retrograde signaling pathways.

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