更新于：2024-11-01

SELENOW

更新于：2024-11-01

基本信息

别名

selenoprotein W、SELENOW、SELW

+ [1]

简介

Plays a role as a glutathione (GSH)-dependent antioxidant. May be involved in a redox-related process. May play a role in the myopathies of selenium deficiency (By similarity).

关联

项与 SELENOW 相关的药物

CN117683798

专利挖掘

靶点

SELENOW

作用机制-

在研机构

中国疾病预防控制中心传染病预防控制所

原研机构

中国疾病预防控制中心传染病预防控制所

在研适应症

肿瘤

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 SELENOW 相关的临床结果

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100 项与 SELENOW 相关的转化医学

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0 项与 SELENOW 相关的专利（医药）

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245

项与 SELENOW 相关的文献（医药）

2024-12-01·Molecular Biology Reports

Selenoprotein W engages in overactive osteoclast differentiation in multiple myeloma

Article

作者: Lee, Kyung Hee ; Oh, Jiin ; Kim, Min Kyoung ; Jeong, Daewon ; Kim, Hyunsoo

AbstractBackgroundPatients with multiple myeloma exhibit malignant osteolytic bone disease due to excessive osteoclast formation and function. We recently identified that osteoclastogenic stimulator selenoprotein W (SELENOW) is upregulated via ERK signaling and downregulated via p38 signaling during receptor activator of nuclear factor (NF)-κΒ ligand (RANKL)-induced osteoclast differentiation. In the intrinsic physiological process, RANKL-induced downregulation of SELENOW maintains proper osteoclast differentiation; in contrast, forced overexpression of SELENOW leads to overactive osteoclast formation and function.Methods and resultsWe observed that SELENOW is highly expressed in multiple myeloma-derived peripheral blood mononuclear cells (PBMCs) and mature osteoclasts when compared to healthy controls. Also, the level of tumor necrosis factor alpha (TNFα), a pathological osteoclastogenic factor, is increased in the PBMCs and serum of patients with multiple myeloma. ERK activation by TNFα was more marked and sustained than that by RANKL, allowing SELENOW upregulation. Excessive expression of SELENOW in osteoclast progenitors and mature osteoclasts derived from multiple myeloma facilitated efficient nuclear translocation of osteoclastogenic transcription factors NF-κB and NFATc1, which are favorable for osteoclast formation.ConclusionOur findings suggest a possibility that feedforward signaling of osteoclastogenic SELENOW by TNFα derived from multiple myeloma induces overactive osteoclast differentiation, leading to bone loss during multiple myeloma.

2024-11-01·Drug Development Research

RNA sequencing comparing centenarian and middle‐aged women lymphoblastoid cell lines identifies age‐related dysregulated expression of genes encoding selenoproteins, heat shock proteins, CD99, and BID

Article

作者: Goldenberg‐Bogner, Ofir ; Israel‐Elgali, Ifat ; Shomron, Noam ; Volkov, Hadas ; Voinsky, Irena ; Puzianowska‐Kuźnicka, Monika ; Gurwitz, David

AbstractWomen typically live longer than men, and constitute the majority of centenarians. We applied RNA‐sequencing (RNA‐seq) of blood‐derived lymphoblastoid cell lines (LCLs) from women aged 60‐80 years and centenarians (100‐105 years), validated the RNA‐seq findings by real‐time PCR, and additionally measured the differentially expressed genes in LCLs from young women aged 20‐35 years. Top RNA‐seq genes with differential expression between the age groups included three selenoproteins (GPX1, SELENOW, SELENOH) and three heat shock proteins (HSPA6, HSPA1A, HSPA1B), with the highest expression in LCLs from young women, indicating that young women are better protected from oxidative stress. The expression of two additional genes, BID encoding BH3‐interacting domain death agonist and CD99 encoding CD99 antigen, showed unique age dependence, with similar expression levels in young and centenarian women while exhibiting higher and lower expression levels, respectively, in LCLs from women aged 60‐80 years compared with the two other age groups. This age‐related differential expression of BID and CD99 suggests elevated inflammation susceptibility in middle‐aged women compared with either young or centenarian women. Our findings, once validated with human peripheral blood mononuclear cells and further cell types, may lead to novel healthy aging diagnostics and therapeutics.

2024-09-20·Science Advances

Loss of SELENOW aggravates muscle loss with regulation of protein synthesis and the ubiquitin-proteasome system

Article

作者: Sun, Lv-Hui ; Niu, Qin-Jian ; Lei, Xin Gen ; Xu, Ze-Jing ; Wei, Jin-Tao ; Liu, Meng ; Huang, Rong-Hui ; Zhao, Ling ; Yang, Jia-Cheng

Sarcopenia is characterized by accelerated muscle mass and function loss, which burdens and challenges public health worldwide. Several studies indicated that selenium deficiency is associated with sarcopenia; however, the specific mechanism remains unclear. Here, we demonstrated that selenoprotein W (SELENOW) containing selenium in the form of selenocysteine functioned in sarcopenia. SELENOW expression is up-regulated in dexamethasone (DEX)–induced muscle atrophy and age-related sarcopenia mouse models. Knockout (KO) of SELENOW profoundly aggravated the process of muscle mass loss in the two mouse models. Mechanistically, SELENOW KO suppressed the RAC1-mTOR cascade by the interaction between SELENOW and RAC1 and induced the imbalance of protein synthesis and degradation. Consistently, overexpression of SELENOW in vivo and in vitro alleviated the muscle and myotube atrophy induced by DEX. SELENOW played a role in age-related sarcopenia and regulated the genes associated with aging. Together, our study uncovered the function of SELENOW in age-related sarcopenia and provides promising evidence for the prevention and treatment of sarcopenia.