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Last update 08 May 2025

SPHKAP

Last update 08 May 2025

Basic Info

Synonyms

A-kinase anchor protein SPHKAP, KIAA1678, SKIP

+ [4]

Introduction

Anchoring protein that binds preferentially to the type I regulatory subunit of c-AMP-dependent protein kinase (PKA type I) and targets it to distinct subcellular compartments. May act as a converging factor linking cAMP and sphingosine signaling pathways. Plays a regulatory role in the modulation of SPHK1.

Drugs associated with SPHKAP

PF-543

Target

SPHKAP

Mechanism

SPHKAP inhibitors

Active Org.

Pfizer Inc.

Originator Org.

Pfizer Inc.

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SPHKAP

100 Translational Medicine associated with SPHKAP

0 Patents (Medical) associated with SPHKAP

Literatures (Medical) associated with SPHKAP

01 May 2025·Journal of Neuroimmunology

Bioinformatics exploration of SPHKAP's role in IDH-mutant glioma involving energy metabolism, prognosis, and immune modulation

Article

Author: Chen, Yuecheng ; Wei, Cuirong ; Qin, Zhongqiao ; Liang, Xi ; Tan, Shi

BACKGROUNDThe current understanding of glioma pathogenesis is limited by the lack of comprehensive insights into the metabolic reprogramming associated with isocitrate dehydrogenase (IDH) mutations. This study aims to contribute a step to this gap by investigating the role of energy metabolism-related genes in glioma. Our objective is to identify key molecular markers that could serve as prognostic markers and potential therapeutic targets for more effective treatment strategies in IDH-mutant glioma patients.METHODSWe conducted an in-depth analysis of gene expression data from TCGA, CGGA, and GEO databases, employing Weighted Gene Co-expression Network Analysis (WGCNA) and differential gene expression analysis to pinpoint candidate genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to elucidate the biological pathways implicated by these genes. Protein-Protein Interaction (PPI) and Gene Multiple Association Network Integration Algorithm (GeneMANIA) networks were constructed to map gene interactions, and survival analysis and Cox regression models were utilized to assess the prognostic value of the identified genes. Additionally, CIBERSORT was used to evaluate immune cell infiltration in the tumor microenvironment.RESULTSOur findings identified SPHKAP as a gene significantly downregulated in glioma tissues compared to control samples. Specifically, low SPHKAP expression was associated with a poorer prognosis of patients with IDH-mutant glioma and linked to the expression of key enzymes involved in energy metabolism. Meanwhile, in IDH-mutant gliomas, reduced SPHKAP expression was correlated with increased macrophage infiltration, enhanced T cell response, and upregulation of immune checkpoint genes, highlighting its role as an independent prognostic marker.CONCLUSIONThis study reveals the differential expression of SPHKAP in glioma, suggesting its potential as a prognostic marker for IDH-mutant gliomas, providing information for future studies aimed at developing targeted therapies for glioma patients.

01 Oct 2024·Journal of Proteomics

DIA proteomic and PRM validation through human granulose cells profiles screen suitable biomarkers for polycystic ovary syndrome patients

Article

Author: Zhang, Ying ; Liu, Faying ; An, Ruifang ; Deng, Wei ; Xu, Xiaoyun ; Zou, Yang ; Tian, Lifeng

The aim of this study is to identify differentially expressed proteins (DEPs) in granulose cells (GCs) from women with or withoutpolycystic ovary syndrome (PCOS) via data independent acquisition (DIA) proteomic analysis.A total of 63 women were recruited for this study, 34 PCOS patients as experimental group (P), and 29 women without PCOS as Normal group (NP). DIA-based proteomic analysis was performed to identify DEPs in GCs between the P and NP samples. Certain typical DEPs were further validated by Parallel reaction monitoring (PRM), and correlation analysis was performed between these DEPs and the clinical characteristics.Cell vitality was measured by CCK-8 assay. DIA analysis revealed 174 significantly DEPs, of which 7 were upregulated and 167 downregulated. Bioinformatics analysis was performed to analysis the significantly DEPs. The PRM experiment confirmed TOP2A and SPHKAP were upregulated significantly in P by comparing to NP, while GM2A, MRPS16, APOA2 and FGF2 were downregulated significantly. Most notably, Correlation analysis revealed that TOP2A, SPHKAP, MRPS16 and FGF2were positively correlated with TG, AMH and Age, but negatively correlated with Menarche age, DBIL, FT3, Basal serum FSH and LH.Meanwhile, CCK-8 assay has shown that downregulation of FGF2 could weaken cell viability. Finally, a panel of DEPs were identified in the GCs of patients with PCOS, of which certain significant DEPs might play essential roles in the pathogenesis of PCOS, could be regarded as candidate biomarkers for PCOS.

01 Apr 2024·Life Sciences

GT-11 impairs insulin signaling through modulation of sphingolipid metabolism in C2C12 myotubes

Article

Author: Roh, Yoon-Seok ; Hong, Jin Tae ; Yoo, Hwan-Soo ; Rustamov, Javokhir

AIMSSphingolipids are involved in the regulation of insulin signaling, which is linked to the development of insulin resistance, leading to diabetes mellitus. We aimed to study whether modulation of sphingolipid levels by GT-11 may regulate insulin signaling in C2C12 myotubes.MAIN METHODSWe investigated the effects of sphingolipid metabolism on Akt phosphorylation and glucose uptake using C2C12 myotubes. Either GT-11, an inhibitor of dihydroceramide desaturase 1 and S1P lyase, or siRNA targeting Sgpl1, the gene encoding the enzyme, was employed to determine the effect of sphingolipid metabolism modulation on insulin signaling. Western blotting and glucose uptake assays were used to evaluate the effect of treatments on insulin signaling. Sphingolipid metabolites were analyzed by high performance liquid chromatography (HPLC).KEY FINDINGSTreatment with GT-11 resulted in decreased Akt phosphorylation and reduced glucose uptake. Silencing the Sgpl1 gene, which encodes S1P lyase, mimicked these findings, suggesting the potential for regulating insulin signaling through S1P lyase modulation. GT-11 modulated sphingolipid metabolism, inducing the accumulation of sphingolipids. Using PF-543 and ARN14974 to inhibit sphingosine kinases and acid ceramidase, respectively, we identified a significant interplay between sphingosine, S1P lyase, and insulin signaling. Treatment with either exogenous sphingosine or palmitic acid inhibited Akt phosphorylation, and reduced S1P lyase activity.SIGNIFICANCEOur findings highlight the importance of close relationship between sphingolipid metabolism and insulin signaling in C2C12 myotubes, pointing to its potential therapeutic relevance for diabetes mellitus.

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SPHKAP

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