Request Demo

Last update 08 May 2025

UBE2E2

Last update 08 May 2025

Basic Info

Synonyms

E2 ubiquitin-conjugating enzyme E2, FLJ25157, UbcH8

+ [5]

Introduction

Accepts ubiquitin from the E1 complex and catalyzes its covalent attachment to other proteins. In vitro catalyzes 'Lys-11'- and 'Lys-48'-, as well as 'Lys-63'-linked polyubiquitination. Catalyzes the ISGylation of influenza A virus NS1 protein.

Drugs associated with UBE2E2

HG-1109

Target

UBE2E2

Mechanism

UBE2E2 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 UBE2E2

100 Translational Medicine associated with UBE2E2

0 Patents (Medical) associated with UBE2E2

129

Literatures (Medical) associated with UBE2E2

01 Apr 2025·Diabetes Research and Clinical Practice

Exploring genetic risk factors for β-cell deterioration in type 2 diabetes mellitus: Insights from longitudinal C-peptide analysis

Article

Author: Matsuoka, Taka-Aki ; Matsuoka, Yuko ; Yamada, Shoichi ; Morita, Shuhei ; Shimajiri, Yoshinori ; Kadoya, Yoshiki ; Sanke, Tokio

AIMSInsulin secretion in type 2 diabetes mellitus deteriorates over time, but the factors influencing the degree of deteriorates remain unclear. This study aims to specifically identify genetic factors associated with this decline.METHODSFasting serum C-peptide was observed over 10.5 ± 4.7 years in 116 Japanese patients with type 2 diabetes mellitus without significant obesity or renal dysfunction. The individual annual decline of fasting serum C-peptide (IAD) was calculated using regression analysis. We evaluated the IAD in patients with or without susceptible allele of candidate single nucleotide polymorphisms (SNPs) in genes (KCNQ1, TCF7L2, CDKN2A/B, CDKAL1, UBE2E2, HHEX, and KCNJ11), which linked to insulin secretion in previous cross-sectional studies.RESULTSThe IAD was -1.513 [-2.635: -0.129] × 10^-2 nmol/L/year. Among the candidate SNPs, only KCNJ11 (rs5219) showed a significant difference in IAD between the patients with homozygous susceptibility allele TT (-2.583 [-3.285: -0.893] × 10^-2 nmol/L/year, N = 20) and those with TC/CC (-1.367 [-2.273: -0.767] × 10^-2 nmol/L/year, N = 96) (P = 0.035).CONCLUSIONSUsing IAD calculated by fasting serum C-peptide over 10 years, KCNJ11 (rs5219) was identified as a genetic factor that was associated with the decline in insulin secretion in Japanese patients with type 2 diabetes mellitus.

01 Mar 2025·Journal of Assisted Reproduction and Genetics

Aneuploidy-driven gene expression profiling in human blastocysts: insights from RNA-Seq analysis

Article

Author: Mohammadi, Reza ; Pazhoomand, Reza ; Bakhtiarizadeh, Mohammad Reza ; Hosseinishenatal, Shirzad ; Khajehoseini, Fattaneh ; Saei, Parishad ; Eftekhari-Yazdi, Poopak ; Gourabi, Hamid ; Bazrgar, Masood

PURPOSEPreimplantation aneuploidy in humans is one of the primary causes of implantation failure and embryo miscarriage. This study was conducted to gain insight into gene expression changes that may result from aneuploidy in blastocysts through RNA-Seq analysis.METHODSThe surplus embryos of preimplantation genetic testing for aneuploidy (PGT-A) candidate couples with normal karyotype and maternal age < 38 were collected following identical ovarian stimulation protocol. The embryos were selected based on trophectoderm biopsy and array comparative genomic hybridization in three groups: normal group, small chromosomes aneuploidy group (SCA), including single aneuploidy for small chromosomes 16, 20, 21, 22, and other chromosomes aneuploidy group (OCA), including single aneuploidy for other chromosomes.RESULTSPrincipal component analysis revealed overall differentiation of transcriptome of the groups, confirming embryo classification. The Gene Ontology indicated that transcription, ubiquitination, autophagy, and DNA repair pathways were upregulated in aneuploid embryos. The overexpression of five genes, UBE2E2 and VPS4A, BUB1B, CDCA8, and COX14 was confirmed by quantitative real-time PCR. Additionally, overexpression was observed in translation and protein synthesis pathways in aneuploid embryos. Mitochondrial pathway upregulation was notable in both SCA and OCA groups, while the apoptosis pathway was overexpressed only in the OCA group. Only cellular lipid synthesis pathway differed between SCA and OCA, the two aneuploid groups.CONCLUSIONSThis study highlights the impact of aneuploidy on the gene expression in blastocysts independent of aneuploidy type and paves the way for understanding the molecular mechanisms underlying the generation of aneuploidy.

23 Jan 2025·JCI Insight

Noncoding variation near UBE2E2 orchestrates cardiometabolic pathophenotypes through polygenic effectors

Article

Author: David, Natalie L ; Chen, Hongyin ; Kumar, G V Naveen ; Qiao, Wanning ; Yang, Jinzhao ; Zhang, Yang ; Steinhauser, Matthew L ; Sharma, Ankit X ; Liu, Silvia ; Pesaresi, Tristan ; Amorim, Tania ; Patel, Kareena ; Andrews, Rosemary E

Mechanisms underpinning signals from genome-wide association studies remain poorly understood, particularly for noncoding variation and for complex diseases such as type 2 diabetes mellitus (T2D) where pathogenic mechanisms in multiple different tissues may be disease driving. One approach is to study relevant endophenotypes, a strategy we applied to the UBE2E2 locus where noncoding single nucleotide variants (SNVs) are associated with both T2D and visceral adiposity (a pathologic endophenotype). We integrated CRISPR targeting of SNV-containing regions and unbiased CRISPR interference (CRISPRi) screening to establish candidate cis-regulatory regions, complemented by genetic loss of function in murine diet-induced obesity or ex vivo adipogenesis assays. Nomination of a single causal gene was complicated, however, because targeting of multiple genes near UBE2E2 attenuated adipogenesis in vitro; CRISPR excision of SNV-containing noncoding regions and a CRISPRi regulatory screen across the locus suggested concomitant regulation of UBE2E2, the more distant UBE2E1, and other neighborhood genes; and compound heterozygous loss of function of both Ube2e2 and Ube2e1 better replicated pathological adiposity and metabolic phenotypes compared with homozygous loss of either gene in isolation. This study advances a model whereby regulatory effects of noncoding variation not only extend beyond the nearest gene but may also drive complex diseases through polygenic regulatory effects.

Analysis

Perform a panoramic analysis of this field.

view full example data

AI Agents Built for Biopharma Breakthroughs

Accelerate discovery. Empower decisions. Transform outcomes.

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

UBE2E2

Basic Info

Related

Analysis