Ask about this productRelated genes to: POLG2 Blocking Peptide
- Gene:
- POLG2 NIH gene
- Name:
- DNA polymerase gamma 2, accessory subunit
- Previous symbol:
- -
- Synonyms:
- MTPOLB, HP55
- Chromosome:
- 17q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-16
- Date modifiied:
- 2016-07-11
Related products to: POLG2 Blocking Peptide
Related articles to: POLG2 Blocking Peptide
- Sex differences in lifespan and age-associated phenotypes are pervasive across species, yet the mechanisms remain poorly understood. Mitochondrial dysfunction is a major hallmark of aging, but whether skeletal muscle mitochondria age along sex specific trajectories remains incompletely defined. - Source: PubMed
Publication date: 2026/04/29
Holcom AngelinaLiao AshleyHolden Kaitlyn GBronikowski Anne MWebb Ashley E - - Source: PubMed
Publication date: 2026/04/07
Peng XuelingLiu Qingdai - N6-methyladenosine (m6A) modification is the most prevalent posttranscriptional epigenetic modification in mammalian mRNAs, and it has been implicated in the regulation of nervous system development by modulating mRNA metabolism. VIRMA is the largest core subunit of the m6A methyltransferase complex and is essential for the assembly and stability of the m6A methyltransferase complex. In the retina, m6A methylation modification is widely distributed in various cellular layers and is essential for retinal homeostasis. Here, we demonstrate that VIRMA-mediated m6A modification is essential for retinal homeostasis. Loss of Virma in retinal rod cells resulted in abnormal reduction in m6A methylation levels, along with impaired photoreceptor function and degeneration. Mechanically, Virma depletion in photoreceptors dampened the m6A modification level of visual perception-associated genes, resulting compromised visual function and photoreceptors degeneration. Moreover, Virma interacted with splicing factor to regulate the alternative splicing events of retina function-related genes such as Polg2, which contributes to photoreceptor damage. Reintroduction of normal Virma expression colonially rescued photoreceptor degeneration. Collectively, our data elucidate the important role of Virma-mediated m6A modification in photoreceptor function and suggest that epigenetic modulation could serve as a potential target to treat these blinding diseases. - Source: PubMed
Publication date: 2026/03/19
Liu WenjingWu XiaojingZou RongZhang FanFan YudiSun KuanxiangYang LipingHu JiangZhang LinZhu Xianjun - - Source: PubMed
Publication date: 2026/01/30
Koch Christian ATüttelmann FrankVedanarayanan Vetta - Mitochondrial genetic diseases are complex disorders that impair cellular energy production, leading to diverse clinical manifestations across multiple organ systems. These diseases arise from mutations in either mitochondrial DNA or nuclear DNA. Among nuclear DNA-related cases, mutations in POLG and POLG2, which encode subunits of mitochondrial DNA polymerase γ, are particularly significant, causing conditions such as Alpers-Huttenlocher syndrome and progressive external ophthalmoplegia. Model organisms have been instrumental in elucidating POLG-related disease mechanisms and advancing therapeutic strategies. Saccharomyces cerevisiae (budding yeast) provided insights into fundamental mitochondrial functions, while Caenorhabditis elegans (roundworm) helped explore POLG's roles in multicellular organisms. Drosophila melanogaster (fruit fly) has been pivotal in studying neurological aspects, and Mus musculus (mouse) models contributed to understanding systemic effects in mammals. Recently, Danio rerio (zebrafish) has emerged as a promising vertebrate model for drug screening, due to its optical transparency and genetic tractability. Each model system offers unique advantages, collectively bridging the gap between basic research and clinical applications. This review will examine in vivo models used in POLG disorder research, highlighting their contributions to understanding disease mechanisms and therapeutic advancements. - Source: PubMed
Publication date: 2025/12/26
Casas Raquel BrañasRisato GiovanniZuppardo AlessandroViscomi CarloArgenton FrancescoDoimo MaraFacchinello NicolaTiso Natascia