Ask about this productRelated genes to: NDNL2 antibody
- Gene:
- NSMCE3 NIH gene
- Name:
- NSE3 homolog, SMC5-SMC6 complex component
- Previous symbol:
- NDNL2
- Synonyms:
- HCA4, MAGEG1, MAGEL3, NSE3
- Chromosome:
- 15q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-19
- Date modifiied:
- 2015-11-19
Related products to: NDNL2 antibody
Related articles to: NDNL2 antibody
- Smc5/6 is a protein complex with a ring structure that suppresses HBV transcription and proliferation. HBV counters this restriction by encoding the regulatory protein HBx, which targets Smc5/6 for proteasomal degradation. However, the molecular mechanism of HBV inhibition by Smc5/6 remains elusive. Here, we take advantage of a luciferase reporter gene in a cell-free expression system and measured the transcriptional activity using the purified Smc5/6 holo-complex, subcomplexes or individual subunits. Besides Smc5/6 holo-complex, NSMCE1/3 subcomplex is sufficient to inhibit transcription in vitro. NSMCE1/3 represses HBx expression at both the mRNA level and the protein level as revealed by the RT-PCR and a cycloheximide chase experiment, respectively. Overexpression of NSMCE1/3 causes degradation of HBx and this effect is blocked by a proteasome inhibitor but not by an inhibitor of the ubiquitin-activating enzyme E1. NSMCE1/3 interacts with the 20S proteasome but does not stimulate the ubiquitination of HBx, indicating that NSMCE1/3 leads to HBx degradation via a ubiquitin-independent proteasomal mechanism. Overexpression of NSMCE1/3 results in inhibition of HBV proliferation in hepatoma cell lines while knockdown of NSMCE3 leads to proliferation promotion. These new findings provide insights into the molecular mechanism of HBV inhibition by Smc5/6. - Source: PubMed
Publication date: 2026/03/11
He LiliShen HuanyuZhao AotingPan YuxuanMa JunOuyang Zhuqing - - Source: PubMed
Chen Chih-Ping - EBV-associated smooth muscle tumour (EBV-SMT) is a rare neoplasm, primarily affecting patients with HIV, post-transplantation (PT), and congenital immunodeficiency (CI). Most EBV-SMT cases were reported by case reports, and genetic analyses are limited. Herein, we describe nine patients with EBV-SMTs to further expand the clinicopathological and genetic spectrum of EBV-SMT. - Source: PubMed
Publication date: 2025/09/16
Jing WenyiRen DanQiu YanQin ShengLan TingHe XinZhang Hongying - - Source: PubMed
Chen LanqinYin JuXu BaopingLiu Xiuyun - We report five patients with lung disease immuno-deficiency and chromosome breakage syndrome (LICS) but without recurrent infections and severe immunodeficiency. One patient had extended survival to 6.5 years. Hematopoietic stem-cell transplantation failed to cure another patient. Our findings suggest that the immunological abnormalities can be limited and do not fully explain the LICS phenotype. - Source: PubMed
Publication date: 2021/03/19
Willemse Brigitte W Mvan der Crabben Saskia NKerstjens-Frederikse Wilhelmina STimens Wimvan Montfrans Joris MLindemans Caroline ABoelens Jaap JanHennus Marije Pvan Haaften Gijs