Редактирование: ILK

Integrin-linked protein kinase (EC 2.7.11.1) (59 kDa serine/threonine-protein kinase) (Beta-integrin-linked kinase) (ILK-1) (ILK-2) (p59ILK) [ILK1] [ILK2]

==Publications==

{{medline-entry
|title=Concurrent nicotine exposure to prenatal alcohol consumption alters the hippocampal and cortical neurotoxicity.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31938742
|abstract=This study investigated the neurotoxic effects of prenatal alcohol and nicotine exposure in the cortex and hippocampus of rodents. Behavioral alterations, electrophysiological changes, and biochemical markers associated with cholinergic neurotransmission, neural oxidative stress, mitochondrial function, and apoptosis were evaluated. Prenatal alcohol exposure induced the generation of ROS, nitrite and lipid peroxide, decreased mitochondrial Complex-I and IV activities, increased Caspase-1 and 3 activities, had no effect on cholinergic neurotransmission, increased expression of [[PSD]]-95, decreased LTP and decreased performance on spatial memory tasks. However, nicotine exposure, in addition to alcohol exposure, was found to mitigate the negative effects of alcohol alone on ROS generation and spatial memory task performances. Furthermore, we also studied the role of [[ILK]] in prenatal alcohol and nicotine exposure. Prenatal Smoking and/or drinking is a major health concern around the world. Thus, our current study may lead to better insights into the molecular mechanisms of fetal alcohol and nicotine exposure on the developing offspring.

|keywords=* Aging
* Mitochondrial function
* Neuroscience
* Oxidative stress
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6953639
}}
{{medline-entry
|title=Age-dependent skeletal muscle transcriptome response to bed rest-induced atrophy.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30605403
|abstract=Short-term muscle disuse induces significant muscle loss in older adults and in some reports may be more accelerated with aging. Identifying muscle transcriptional events in response to bed rest may help identify therapeutic targets to offset muscle loss. Therefore, we compared the muscle transcriptome between young and older adults after bed rest and identified candidate targets related to changes in muscle loss. RNA was sequenced (HiSeq, Illumina; DESeq, R) from muscle biopsies obtained from young [ n = 9; 23 yr (SD 3)] and older [ n = 18; 68 yr (SD 6)] adults before and after 5-day bed rest. Significantly altered pathways in both young and old subjects relating to mechanosensing and cell adhesion (Actin Cytoskeleton Signaling, [[ILK]] Signaling, RhoA Signaling, and Integrin Signaling) were altered (activation z score) to a greater extent in old subjects. Hepatic Fibrosis/Hepatic Stellate Cell Activation was the top regulated pathway significantly altered only in the old. Fifty-one differentially regulated genes were only altered in the young after bed rest and resembled a gene expression profile like that in the old at baseline. Inflammation and muscle wasting genes (CXCL2, GADD45A) were uniquely increased in the old after bed rest, and the macrophage gene [[MAFB]] decreased in the old and correlated with the change in leg lean mass. In summary, skeletal muscle dysregulation during bed rest in the old may be driven by alterations in molecules related to fibrosis, inflammation, and cell adhesion. This information may aid in the development of mechanistic-based therapies to combat muscle atrophy during short-term disuse. NEW