CDS2

Last update 08 May 2025

Basic Info

Synonyms

CDP-DAG synthase 2, CDP-DG synthase 2, CDP-diacylglycerol synthase 2

+ [6]

Introduction

Catalyzes the conversion of phosphatidic acid (PA) to CDP-diacylglycerol (CDP-DAG), an essential intermediate in the synthesis of phosphatidylglycerol, cardiolipin and phosphatidylinositol (PubMed:25375833). Exhibits specificity for the nature of the acyl chains at the sn-1 and sn-2 positions in the substrate, PA and the preferred acyl chain composition is 1-stearoyl-2-arachidonoyl-sn-phosphatidic acid (PubMed:25375833). Plays an important role in regulating the growth and maturation of lipid droplets which are storage organelles at the center of lipid and energy homeostasis (PubMed:26946540, PubMed:31548309).

100 Clinical Results associated with CDS2

100 Translational Medicine associated with CDS2

0 Patents (Medical) associated with CDS2

Literatures (Medical) associated with CDS2

01 Jan 2025·Veterinary Medicine and Science

Comparative Analysis of Runs of Homozygosity Islands in Indigenous and Commercial Chickens Revealed Candidate Loci for Disease Resistance and Production Traits

Article

Author: Rostamzadeh Mahdabi, Elaheh ; Han, Jianlin ; Esmailizadeh, Ali ; Wang, Ming‐Shan

ABSTRACTRuns of homozygosity (ROH) are contiguous stretches of identical genomic regions inherited from both parents. Assessment of ROH in livestock species contributes significantly to our understanding of genetic health, population genetic structure, selective pressure and conservation efforts. In this study, whole genome re‐sequencing data from 140 birds of 10 Iranian indigenous chicken ecotypes, 3 commercial chicken breeds and 1 red junglefowl (RJF) population were used to investigate their population genetic structure, ROH characteristics (length and frequency) and genomic inbreeding coefficients (FROH). Additionally, we examined ROH islands for selection footprints in the indigenous chicken populations. Our results revealed distinct genetic backgrounds, among which the White Leghorn breed exhibited the greatest genetic distance from other populations, while the gamecock populations formed a separate cluster. We observed significant differences in ROH characteristics, in which the commercial breeds showed a higher number of ROH compared to indigenous chickens and red junglefowls. Short ROH ranging from 0.1 to 1 Mb were dominant among the populations. The Arian line had the highest mean length of ROH, while the White Leghorn breed showed the highest number of ROH. Among indigenous chickens, the Lari‐Afghani ecotype exhibited the highest FROH, but the Sari inherited the richest genetic diversity. Interestingly, GGA16 carried no ROH in the red junglefowls, whereas GGA22 had the highest FROH across all populations, except in the Isfahan ecotype. We also identified ROH islands associated with genetic adaptations in indigenous ecotypes. These islands harboured immune‐related genes contributing to disease resistance (TLR2, TICAM1, IL22RA1, NOS2, CCL20 and IFNLR1), heat tolerance and oxidative stress response (NFKB1, HSF4, OSGIN1 and BDNF), and muscle development, lipid metabolism and reproduction (MEOX2, CEBPB, CDS2 and GnRH‐I). Overall, this study highlights the genetic potential of indigenous chickens to survive and adapt to their respective environments.

01 Dec 2024·The Journal of Prevention of Alzheimer's Disease

Quantifying Personalized Shift-Work Molecular Portraits Underlying Alzheimer's Disease through Computational Biology

Article

Author: Fu, T. ; Gong, Z. ; Yuan, P. ; Jing, L ; Jia, Y. ; Liu, H ; Zhang, G ; Zhou, Z ; Yao, Y. ; Li, Y. ; Qin, H. ; Jing, L. ; Wang, R. ; Yang, L. ; Xu, Y. ; Yang, L ; Li, Q ; Li, Y ; Peng, T. ; Cai, Z ; Fu, T ; Wang, R ; Cai, Z. ; Zhao, X ; Gong, Z ; Liu, H. ; Peng, T ; Qin, H ; Yuan, P ; Jia, Y ; Xu, Y ; Li, Q. ; Zhou, Z. ; Yao, Y ; Zhang, G. ; Zhao, X.

BACKGROUNDShift work, the proven circadian rhythm-disrupting behavior, has been linked to the increased risk of Alzheimer's disease (AD). However, the putative causal effect and potential mechanisms of shift work for AD were still unclear.METHODSMendelian randomization (MR) analysis was performed to discover the putative causal effect of shift work for AD. Expression quantitative trait loci (eQTLs) and transcriptome data were integrated to identify genes causally associated with AD from circadian-related genes. An in vitro experiment was also conducted to validate the expression of target genes. Based on the identified genes, a novel integrative program and 4,077 samples from 16 microarray datasets were leveraged to assess the extent of circadian rhythm disruption (CRD), defined as the clock deviation level (CDL).FINDINGS/RESULTSShift work causally increased the risk of AD [odds ratio (OR) = 2.49, 95% CI = 1.79 - 3.19, p = 0.01]. Seven circadian-related genes were causally associated with AD, including CCS, CDS2, MYRIP, NRP1, PLEKHA5, POLR1D, and PPP4C. These genes were significantly correlated with the circadian rhythm pathway. CDL was higher in CRD mice group, shift work group, sleep restriction group, and AD patients compared to control mice group (p = 0.043), non-shift group (p = 0.004), sleep extension group (p = 0.025), and health controls (multiple cohorts, p < 0.05). Additionally, CDL was also significantly correlated with AD's clinical biomarkers.INTERPRETATIONS/CONCLUSIONBy combining GWAS and transcriptome data, this study demonstrated the causal role of CRD behavior in AD, identified the potential target genes in shift work-induced AD, and generated CDL to characterize CRD status, which provided evidence and prospects for disease prevention and future therapeutic interventions.

16 Oct 2024·Biochemical Journal

CDS2 expression regulates de novo phosphatidic acid synthesis

Article

Author: Janardan, Vishnu ; Anderson, Karen E. ; Lopez-Clavijo, Andrea F. ; Walker, Simon ; Raghu, Padinjat ; Barneda, David ; Hawkins, Phillip T. ; Taylor, Diane ; Stephens, Len R. ; Collins, Daniel M. ; Qiu, Danye ; Jessen, Henning J. ; Clark, Jonathan ; Niewczas, Izabella

CDS enzymes (CDS1 and 2 in mammals) convert phosphatidic acid (PA) to CDP-DG, an essential intermediate in the de novo synthesis of PI. Genetic deletion of CDS2 in primary mouse macrophages resulted in only modest changes in the steady-state levels of major phospholipid species, including PI, but substantial increases in several species of PA, CDP-DG, DG and TG. Stable isotope labelling experiments employing both 13C6- and 13C6D7-glucose revealed loss of CDS2 resulted in a minimal reduction in the rate of de novo PI synthesis but a substantial increase in the rate of de novo PA synthesis from G3P, derived from DHAP via glycolysis. This increased synthesis of PA provides a potential explanation for normal basal PI synthesis in the face of reduced CDS capacity (via increased provision of substrate to CDS1) and increased synthesis of DG and TG (via increased provision of substrate to LIPINs). However, under conditions of sustained GPCR-stimulation of PLC, CDS2-deficient macrophages were unable to maintain enhanced rates of PI synthesis via the ‘PI cycle’, leading to a substantial loss of PI. CDS2-deficient macrophages also exhibited significant defects in calcium homeostasis which were unrelated to the activation of PLC and thus probably an indirect effect of increased basal PA. These experiments reveal that an important homeostatic response in mammalian cells to a reduction in CDS capacity is increased de novo synthesis of PA, likely related to maintaining normal levels of PI, and provides a new interpretation of previous work describing pleiotropic effects of CDS2 deletion on lipid metabolism/signalling.

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CDS2

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