日期:
2020 年 — 2026 年
2020
2021
2022
2023
2024
2025
2026
影响因子:

Hemizygous mutation of Jmjd3 in muscle stem cells increases H3K27 methylation on Pax7 leading to impaired myogenesis

肌肉干细胞中Jmjd3的半合子突变会增加Pax7上的H3K27甲基化,从而导致肌生成受损。

Tidball, James G; Petrossian, Lina; McKee, Cynthia M; Wehling-Henricks, Michelle

Aging of the immune system and impaired muscle regeneration: A failure of immunomodulation of adult myogenesis

免疫系统衰老和肌肉再生受损:成人肌生成免疫调节失败

Tidball, James G; Flores, Ivan; Welc, Steven S; Wehling-Henricks, Michelle; Ochi, Eisuke

Myeloid cell-derived tumor necrosis factor-alpha promotes sarcopenia and regulates muscle cell fusion with aging muscle fibers

髓系细胞衍生的肿瘤坏死因子-α促进肌肉减少症,并调节肌肉细胞与衰老肌肉纤维的融合。

Wang, Ying; Welc, Steven S; Wehling-Henricks, Michelle; Tidball, James G

Immunobiology of Inherited Muscular Dystrophies

遗传性肌营养不良症的免疫生物学

Tidball, James G; Welc, Steven S; Wehling-Henricks, Michelle

Macrophages escape Klotho gene silencing in the mdx mouse model of Duchenne muscular dystrophy and promote muscle growth and increase satellite cell numbers through a Klotho-mediated pathway

在杜氏肌营养不良症的mdx小鼠模型中,巨噬细胞能够逃脱Klotho基因沉默,并通过Klotho介导的通路促进肌肉生长并增加卫星细胞数量。

Wehling-Henricks, Michelle; Welc, Steven S; Samengo, Guiseppina; Rinaldi, Chiara; Lindsey, Catherine; Wang, Ying; Lee, Jeongyoon; Kuro-O, Makoto; Tidball, James G

Klotho gene silencing promotes pathology in the mdx mouse model of Duchenne muscular dystrophy

Klotho基因沉默会促进杜氏肌营养不良症mdx小鼠模型的病理发展

Wehling-Henricks, Michelle; Li, Zhenzhi; Lindsey, Catherine; Wang, Ying; Welc, Steven S; Ramos, Julian N; Khanlou, Négar; Kuro-O, Makoto; Tidball, James G

Increases of M2a macrophages and fibrosis in aging muscle are influenced by bone marrow aging and negatively regulated by muscle-derived nitric oxide

衰老肌肉中M2a巨噬细胞增多和纤维化受骨髓衰老的影响,并受肌肉源性一氧化氮的负调控。

Wang, Ying; Wehling-Henricks, Michelle; Samengo, Giuseppina; Tidball, James G

Nitric oxide synthase deficiency and the pathophysiology of muscular dystrophy

一氧化氮合酶缺乏症与肌营养不良症的病理生理学

Tidball, James G; Wehling-Henricks, Michelle

Loss of positive allosteric interactions between neuronal nitric oxide synthase and phosphofructokinase contributes to defects in glycolysis and increased fatigability in muscular dystrophy.

神经元一氧化氮合酶和磷酸果糖激酶之间正向变构相互作用的丧失会导致肌肉营养不良症中糖酵解缺陷和疲劳感增加

Wehling-Henricks Michelle, Oltmann Meredith, Rinaldi Chiara, Myung Kyu H, Tidball James G

Major basic protein-1 promotes fibrosis of dystrophic muscle and attenuates the cellular immune response in muscular dystrophy

主要碱性蛋白-1促进营养不良肌肉的纤维化,并减弱肌营养不良症中的细胞免疫反应。

Wehling-Henricks, Michelle; Sokolow, Sophie; Lee, Jamie J; Myung, Kyu H; Villalta, S Armando; Tidball, James G