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Role of Nonhistone Chromosomal Proteins in Selective Gene Expression
Published in Gerald M. Kolodny, Eukaryotic Gene Regulation, 2018
I.R. Phillips, E.A. Shephard, J.L. Stein, G.S. Stein
Nonhistone chromosomal proteins can undergo several types of postsynthetic modification. Radioactive labeling and composition analysis experiments have shown that they can be acetylated49–51 and methylated.52–54 Acetyl CoA serves as the prinicipal acetate donor and S-adenosyl methionine as the primary source of methyl groups. There is also evidence that the thiol groups of nonhistone proteins can undergo rearrangements.55–57 These proteins can also undergo amino-terminal arginylation by argi-nyl-tRNA.58
Molecular mechanism analysis of m6A modification-related lncRNA-miRNA-mRNA network in regulating autophagy in acute pancreatitis
Published in Islets, 2022
Xiang Li, Hong Qin, Ali Anwar, Xingwen Zhang, Fang Yu, Zheng Tan, Zhanhong Tang
Tsc1 and other genes are closely related to autophagy and play a certain role in AP. Mechanistically, Tsc1 deficiency led to autophagy suppression45 and a direct connection between Raf-1 activation and cellular autophagy.46 Rong Y et al. found that resveratrol can protect rats against SAP by activating the Sirt1-FoxO1 axis,47 consistent with the key pathways found in this project. The activation of the Sirt1-autophagy signaling pathway alleviates AP.48 Research shows that more severe chronic pancreatitis is associated with significantly increased Hspa5 mRNA levels.49 Crosstalk between Hspa5 arginylation and sequential ubiquitination leads to AKT degradation through autophagy flux.50 In addition, the increased immunohistochemical expression of Vegfa can play an important role in tracking the evolution and pathology of AP.51 Several studies have shown that Vegfa is closely related to autophagy.52–54 Overexpression of c-Fos increased the Beclin1-induced autophagy.55 Ultimately, Parp1 is a key regulator of cell death. Its inhibition prevented streptozotocin-induced diabetes and attenuated caerulein-induced AP.56 The targeted inhibition of Pten expression in AP can induce acinar cell apoptosis and inhibit inflammatory response.57 Pten phosphorylation promotes its nuclear translocation and autophagy, but the role of Pten in acinar cell autophagy is not clear.58 In general, some studies have shown the potential function of the above key genes in AP.
When nature’s robots go rogue: exploring protein homeostasis dysfunction and the implications for understanding human aging disease pathologies
Published in Expert Review of Proteomics, 2018
Julie A. Reisz, Alexander S. Barrett, Travis Nemkov, Kirk C. Hansen, Angelo D’Alessandro
Chaperones and proteolysis systems are profoundly affected during aging. HSR repression begins at the onset of reproductive maturity in Caenorhabditis elegans (C. elegans) via epigenetic modification of histone H3 [69]. Both the UPS and the lysosomal system have diminished proteolysis capacities in aging organisms and their protein machineries are each susceptible to aging-related damage through oxidation, conjugation to lipid peroxidation products [70], and/or protein cross-linking [71–73]. Though spatially distinct, the lysosome and proteasome are interrelated and have been shown to compensate, at least partially, when one is compromised [74,75]. One example of this interplay was revealed in a study earlier this year of N-terminal arginylation, in which arginine is added to specific residues of protein N-termini exposed by endopeptidase activity. Though a comprehensive picture of the cellular consequences of arginylation is not yet established, experiments in this study found that proteins containing this modification are detected by N-recognins that direct the protein to the UPS or, when the UPS is inhibited or compromised, by p62 with resulting autophagy [76]. Such observations illustrate compensatory mechanisms within proteostasis and how damaged or dysfunctional proteins may be processed differentially in context-dependent manners. Further illustrating the interconnections between these two proteolytic hubs, the transcription factor homeodomain-interacting protein kinase 1 (HPK-1) was recently identified as preserving proteostasis in C. elegans by both suppressing an inhibitory posttranslational modification to HSF-1 and, separately, by regulating the expression of genes involved in the autophagy pathway, particularly autophagosome formation [77].
Child with cerebral malformations and epilepsy
Published in International Journal of Neuroscience, 2018
Ying Sun, Xuehua Shen, Qiubo Li, Qingxia Kong
Actin encoded by the ACTB (βcyto-actin) gene is commonly expressed in vertebrates [8]. Actins are highly conserved proteins that are involved in cell motility, structure, integrity and intercellular signalling. The encoded protein is a major constituent of the contractile apparatus and one of the two nonmuscle cytoskeletal actins that are ubiquitously expressed. Additionally, post-translational modification by arginylation of βcyto-actin helps cellular activity and increases actin polymerization [9].