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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Sequential phosphorylation of CCAAT enhancer-binding protein beta by MAPK and glycogen synthase kinase 3 beta is required for adipogenesis
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Sequential phosphorylation of CCAAT enhancer-binding protein beta by MAPK and glycogen synthase kinase 3 beta is required for adipogenesis

机译：MAPK和糖原合酶激酶3 beta对CCAAT增强剂结合蛋白β的顺序磷酸化是脂肪形成所必需的

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摘要

CCAAT enhancer-binding protein (C/EBP)beta, C/EBP alpha, and peroxisome proliferator activated receptor (PPAR)gamma act in a cascade where C/EBP beta activates expression of C/EBP alpha and PPAR gamma, which then function as pleiotropic activators of genes that produce the adipocyte phenotype. When growth-arrested 3T3-L1 preadipocytes are induced to differentiate, C/EBP beta is rapidly expressed but still lacks DNA-binding activity. After a long (14-hour) lag, glycogen synthase kinase 313 enters the nucleus, which correlates with hyperphosphorylation of C/EBP beta and acquisition of DNA-binding activity. Concurrently, 3T3-L1 preadipocytes synchronously enter S phase and undergo mitotic clonal expansion, a prerequisite for terminal differentiation. Ex vivo and in vitro experiments with C/EBP beta show that phosphorylation of Thr-188 by mitogen-activating protein kinase "primes" C/EBP beta for subsequent phosphorylation on Ser-184 and Thr-179 by glycogen synthase kinase 30, acquisition of DNA-binding function, and transactivation of the C/EBP alpha and PPAR gamma genes. The delayed transactivation of the C/EBP alpha and PPAR gamma genes by C/EBP beta appears necessary to allow mitotic clonal expansion, which would otherwise be prevented, because C/EBP alpha and PPAR-gamma are antimitotic.
机译：CCAAT增强子结合蛋白（C / EBP）β，C / EBPα和过氧化物酶体增殖物激活受体（PPAR）γ共同起作用，其中C / EBPβ激活C / EBPα和PPARγ的表达，然后作为产生脂肪细胞表型的基因的多效激活剂。当诱导生长停滞的3T3-L1前脂肪细胞分化时，C / EBPβ迅速表达，但仍缺乏DNA结合活性。经过长时间（14小时）的滞后后，糖原合酶激酶313进入细胞核，该细胞核与C / EBPβ的过度磷酸化和DNA结合活性的获得有关。同时，3T3-L1前脂肪细胞同步进入S期并经历有丝分裂克隆扩增，这是终末分化的前提。用C / EBPβ进行的离体和体外实验表明，丝裂原激活蛋白激酶“引发”了Thr-188的磷酸化，随后糖原合酶激酶30在Ser-184和Thr-179上磷酸化了C / EBPβ， DNA结合功能，以及C / EBPα和PPARγ基因的反式激活。 C / EBP beta延迟C / EBP alpha和PPAR gamma基因的反式激活似乎是允许有丝分裂克隆扩张的必要条件，否则将被阻止，因为C / EBP alpha和PPAR-γ是抗有丝分裂的。

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