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首页> 外文期刊>American Journal of Physiology >Cloning and characterization of mouse 5'-AMP-activated protein kinase gamma3 subunit.
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Cloning and characterization of mouse 5'-AMP-activated protein kinase gamma3 subunit.

机译：小鼠5'-AMP激活的蛋白激酶gamma3亚基的克隆和表征。

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Naturally occurring mutations in the regulatory gamma-subunit of 5'-AMP-activated protein kinase (AMPK) can result in pronounced pathological changes that may stem from increases in muscle glycogen levels, making it critical to understand the role(s) of the gamma-subunit in AMPK function. In this study we cloned the mouse AMPKgamma3 subunit and revealed that there are two transcription start sites, which result in a long form, gamma3L (AF525500) and a short form, gamma3S (AF525501). AMPKgamma3L is the predominant form in mouse and is specifically expressed in mouse skeletal muscle at the protein level. In skeletal muscle, AMPKgamma3 shows higher levels of expression in fast-twitch white glycolytic muscle (type IIb) compared with fast-twitch red oxidative glycolytic muscle (type IIa), whereas gamma3 is undetectable in soleus muscle, a slow-twitch oxidative muscle with predominantly type I fibers. AMPKgamma3 can coimmunoprecipititate with both alpha and beta AMPK subunits. Overexpression of gamma3S and gamma3L in mouse tibialis anterior muscle in vivo has no effect on alpha1 and alpha2 subunit expression and does not alter AMPKalpha2 catalytic activity. However, gamma3S and gamma3L overexpression significantly increases AMPKalpha1 phosphorylation and activity by approximately 50%. The increase in AMPKalpha1 activity is not associated with alterations in glycogen accumulation or glycogen synthase expression. In conclusion, the gamma3 subunit of AMPK is highly expressed in fast-twitch glycolytic skeletal muscle, and wild-type gamma3 functions in the regulation of alpha1 catalytic activity, but it is not associated with changes in muscle glycogen concentrations.
机译：5'-AMP激活的蛋白激酶（AMPK）的调节性γ亚基中自然发生的突变可导致明显的病理变化，其可能源于肌肉糖原水平的升高，因此了解γ的作用至关重要AMPK功能中的-subunit。在这项研究中，我们克隆了小鼠AMPKgamma3亚基，并揭示了两个转录起始位点，它们形成一个长形式的gamma3L（AF525500）和一个短形式的gamma3S（AF525501）。 AMPKgamma3L是小鼠的主要形式，并在蛋白质水平上在小鼠骨骼肌中特异性表达。在骨骼肌中，AMPKgamma3在快速抽搐的白色糖酵解肌（IIb型）中比在快速抽搐的红色氧化糖酵解肌（IIa型）中表达更高，而在比目鱼肌中则无法检测到gamma3，比目鱼肌是一种缓慢抽搐的氧化性肌主要是I型纤维。 AMPKgamma3可以与alpha和βAMPK亚基共免疫沉淀。体内小鼠胫前肌中γ3S和γ3L的过表达对α1和α2亚基表达没有影响，并且不会改变AMPKalpha2的催化活性。但是，gamma3S和gamma3L过表达会显着增加AMPKalpha1的磷酸化和活性约50％。 AMPKalpha1活性的增加与糖原积累或糖原合酶表达的改变无关。总之，AMPK的gamma3亚基在快速抽搐的糖酵解骨骼肌中高表达，野生型gamma3在调节alpha1催化活性中起作用，但与肌肉糖原浓度的变化无关。

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