NRAS palmitoylation and oncogenic fitness

Castilla, Lucio H.

doi:10.1182/blood.2020005720

Cited by 3 publications

(4 citation statements)

References 11 publications

(18 reference statements)

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“…Those point mutations might play a role in disease progression and pathogenesis [ 25 ]. GeneMANIA analysis revealed that FOXP4 gene significantly interacts with 20 different genes [ [47] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] , [59] , [60] , [61] , [62] , [63] , [64] , [65] , [66] ]. FOXP4 gene showed more significant interactions with FOXP1, 2 genes, MKI67 (marker of proliferation Ki-67), GATAD2B (GATA zinc finger domain containing 2B) than others genes.…”

Section: Discussionmentioning

confidence: 99%

Prediction and assessment of deleterious and disease causing nonsynonymous single nucleotide polymorphisms (nsSNPs) in human FOXP4 gene: An in-silico study

Kamal,

Teeya,

Rahman

et al. 2024

Heliyon

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Section: Discussionmentioning

confidence: 99%

Prediction and assessment of deleterious and disease causing nonsynonymous single nucleotide polymorphisms (nsSNPs) in human FOXP4 gene: An in-silico study

Kamal,

Teeya,

Rahman

et al. 2024

Heliyon

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“…The effect of palmitoylation on tumorigenesis is mostly through the modification of key molecules (EGFR, RAS, etc.) of tumor proliferation, death resistance, and tumor metastasis, causing abnormalities in signaling pathways, metabolism, and gene expression regulation [ 31 , 32 ]. However, our results showed that the change in GSK3β palmitoylation did not affect the level of β-catenin.…”

Section: Discussionmentioning

confidence: 99%

GSK3β palmitoylation mediated by ZDHHC4 promotes tumorigenicity of glioblastoma stem cells in temozolomide-resistant glioblastoma through the EZH2–STAT3 axis

Zhao

Fan

et al. 2022

Oncogenesis

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Glioblastoma stem cells (GSCs) are a highly tumorigenic cell subgroup of glioblastoma (GBM). Glycogen synthase kinase 3β (GSK3β) is considered a key hub for promoting malignant phenotypes in GBM. However, the functional relationships between GSK3β and GSCs in GBM are unclear. Here, we found that GSK3β was noted as a substrate for ZDHHC4-mediated palmitoylation at the Cys14 residue, which enhanced GBM temozolomide (TMZ) resistance and GSC self-renewal. Clinically, the expression level of ZDHHC4 was upregulated in GBM, which significantly correlated with tumor grade and poor prognosis. The above phenotypes were based on decreasing p-Ser9 and increasing p-Tyr216 by GSK3β palmitoylation, which further activated the enhancer of the zeste homolog 2 (EZH2)–STAT3 pathway. Notably, STAT3 silencing also inhibited ZDHHC4 expression. This study revealed that GSK3β palmitoylation mediated by ZDHHC4 improved the stemness of TMZ-resistant GBM by activating the EZH2–STAT3 signaling axis, providing a new theoretical basis for further understanding the mechanism of TMZ resistance and recurrence after treatment.

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“…Cellular palmitoylation maintains a dynamic balance to ensure normal life activities, and any disruptions of this balance can lead to various diseases, such as autoimmune diseases, 613 neurodegenerative diseases, 593 T2DM, 33 and nonalcoholic fatty liver disease, 677 tumors, 680 , 681 , 682 , 683 Friedreich ataxia, and peripheral artery disease. 684 , 685 Elevated palmitoylation of NOD2 mutants in autoinflammatory diseases leads to inflammation and inhibits autophagic degradation (Figure 11 ).…”

Section: Long‐chain Fatty Acid Modificationsmentioning

confidence: 99%

“…678 In addition, the palmitoyltransferase ZDHHC5 mediates the palmitoylation of NOD1/2 to promote its membrane recruitment and immune signaling, which are extremely important for microorganisms to establish an effective immune response. 679 Cellular palmitoylation maintains a dynamic balance to ensure normal life activities, and any disruptions of this balance can lead to various diseases, such as autoimmune diseases, 613 neurodegenerative diseases, 593 T2DM, 33 and nonalcoholic fatty liver disease, 677 tumors, [680][681][682][683] Friedreich ataxia, and peripheral artery disease. 684,685 Elevated palmitoylation of NOD2 mutants in autoinflammatory diseases leads to inflammation and inhibits autophagic degradation (Figure 11).…”

Section: Palmitoylationmentioning

confidence: 99%

Protein posttranslational modifications in health and diseases: Functions, regulatory mechanisms, and therapeutic implications

Zhong

Xiao

Xie

et al. 2023

MedComm

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Protein posttranslational modifications (PTMs) refer to the breaking or generation of covalent bonds on the backbones or amino acid side chains of proteins and expand the diversity of proteins, which provides the basis for the emergence of organismal complexity. To date, more than 650 types of protein modifications, such as the most well‐known phosphorylation, ubiquitination, glycosylation, methylation, SUMOylation, short‐chain and long‐chain acylation modifications, redox modifications, and irreversible modifications, have been described, and the inventory is still increasing. By changing the protein conformation, localization, activity, stability, charges, and interactions with other biomolecules, PTMs ultimately alter the phenotypes and biological processes of cells. The homeostasis of protein modifications is important to human health. Abnormal PTMs may cause changes in protein properties and loss of protein functions, which are closely related to the occurrence and development of various diseases. In this review, we systematically introduce the characteristics, regulatory mechanisms, and functions of various PTMs in health and diseases. In addition, the therapeutic prospects in various diseases by targeting PTMs and associated regulatory enzymes are also summarized. This work will deepen the understanding of protein modifications in health and diseases and promote the discovery of diagnostic and prognostic markers and drug targets for diseases.

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NRAS palmitoylation and oncogenic fitness

Cited by 3 publications

References 11 publications

Prediction and assessment of deleterious and disease causing nonsynonymous single nucleotide polymorphisms (nsSNPs) in human FOXP4 gene: An in-silico study

Prediction and assessment of deleterious and disease causing nonsynonymous single nucleotide polymorphisms (nsSNPs) in human FOXP4 gene: An in-silico study

GSK3β palmitoylation mediated by ZDHHC4 promotes tumorigenicity of glioblastoma stem cells in temozolomide-resistant glioblastoma through the EZH2–STAT3 axis

Protein posttranslational modifications in health and diseases: Functions, regulatory mechanisms, and therapeutic implications

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