无所不在
MAPK/ERK通路
病因学
生物
信号转导
表达式(计算机科学)
量子纠缠
癌症研究
医学
癌症
基因表达
病理
遗传学
基因
内科学
哲学
物理
计算机科学
量子
认识论
量子力学
程序设计语言
作者
Joydeep Chakraborty,Sayan Chakraborty,Sohag Chakraborty,Mahesh Narayan
标识
DOI:10.1016/j.bbagrm.2023.194988
摘要
Mitogen Activated Protein Kinase (MAPK) is one of the most well characterized cellular signaling pathways that controls fundamental cellular processes including proliferation, differentiation, and apoptosis. These cellular functions are consequences of transcription of regulatory genes that are influenced and regulated by the MAP-Kinase signaling cascade. MAP kinase components such as Receptor Tyrosine Kinases (RTKs) sense external cues or ligands and transmit these signals via multiple protein complexes such as RAS–RAF, MEK, and ERKs and eventually modulate the transcription factors inside the nucleus to induce transcription and other regulatory functions. Aberrant activation, dysregulation of this signaling pathway, and genetic alterations in any of these components results in the developmental disorders, cancer, and neurodegenerative disorders. Over the years, the MAPK pathway has been a prime pharmacological target, to treat complex human disorders that are genetically linked such as cancer, Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. The current review re-visits the mechanism of MAPK pathways in gene expression regulation. Further, a current update on the progress of the mechanistic understanding of MAPK components is discussed from a disease perspective.
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