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Last update 08 May 2025

ACAA1

Last update 08 May 2025

Basic Info

Synonyms

3-ketoacyl-CoA thiolase, peroxisomal, ACAA, ACAA1

+ [7]

Introduction

Responsible for the thiolytic cleavage of straight chain 3-keto fatty acyl-CoAs (3-oxoacyl-CoAs) (PubMed:11734571, PubMed:2882519). Plays an important role in fatty acid peroxisomal beta-oxidation (PubMed:11734571, PubMed:2882519). Catalyzes the cleavage of short, medium, long, and very long straight chain 3-oxoacyl-CoAs (PubMed:11734571, PubMed:2882519).

Drugs associated with ACAA1

KN-510713

Target

ACAA1 x SLC25A20

Mechanism

ACAA1 inhibitors [+1]

Active Org.

National Cancer Center Korea [+1]

Originator Org.

New Cancer Cure-Bio Co.,Ltd.

Active Indication

Pancreatic Cancer

Inactive Indication-

Drug Highest PhasePhase 1/2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

KN-713

Target

ACAA1

Mechanism

ACAA1 inhibitors

Active Org.

National Cancer Center Korea [+1]

Originator Org.

New Cancer Cure-Bio Co.,Ltd.

Active Indication

Advanced Malignant Solid Neoplasm [+1]

Inactive Indication-

Drug Highest PhasePhase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with ACAA1

NCT06012708

/ CompletedPhase 1

An Open-label, Dose-escalation and Dose-finding, Phase 1 Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of KN510, KN713 as Combination Therapy in Patients With Advanced Solid Tumors

To evaluate the safety and tolerability of the combination therapy of KN510 and KN713 and determine the MTD and RP2D in patients with advanced solid tumors.

Start Date11 Sep 2023

Sponsor / Collaborator

New Cancer Cure-Bio Co.,Ltd.

100 Clinical Results associated with ACAA1

100 Translational Medicine associated with ACAA1

0 Patents (Medical) associated with ACAA1

283

Literatures (Medical) associated with ACAA1

01 Feb 2025·Environmental Research

Prenatal bisphenol analogs exposure and placental DNA hypomethylation of genes in the PPAR signaling pathway: Insights for bisphenol analogs’ effects on infant anthropometry

Article

Author: Wu, Qihan ; Ji, Honglei ; Zhu, Haijun ; Yuan, Zhengwei ; Chen, Yao ; Liu, Xiao ; Wang, Ziliang ; Miao, Maohua ; Yuan, Wei ; Liang, Hong

Prenatal exposure to bisphenol analogs (BPs) may pose hazards to offspring's health; however, their underlying mechanisms remain to be elucidated. DNA methylation, a major epigenetic mechanism, may be involved in early programming following environmental disturbances. In this prospective study, we investigated associations between prenatal BPs exposure and the placental DNA methylation levels of 14 candidate genes in the peroxisome proliferator-activated receptor (PPAR) signaling pathway among 205 mother-infant pairs and explored the potential mediating role of the DNA methylation in the association of prenatal BPs exposure with anthropometric measurements of infants aged 1 year. We observed a general pattern that prenatal BPs exposure was associated with the DNA hypomethylation of candidate genes, with associations consistently and notably observed for PPAR α (PPARA), retinoid X receptor α (RXRA), acetyl-CoA acyltransferase 1, and acyl-CoA dehydrogenase medium chain (ACADM) in linear regression and Bayesian kernel machine regression. Both models identified bisphenol F (BPF) as the predominant compound. We found inverse associations between the placental DNA methylation levels of most candidate genes, such as PPARA, RXRA, ACADM, and nuclear receptor subfamily 1 group H member 3 (NR1H3), and the length-for-age z-score, arm circumference-for-age z-score, subscapular skinfold-for-age z-score, and abdominal skinfold thickness of the infants. The DNA methylation levels of RXRA and NR1H3 could mediate the associations between prenatal BPF exposure and increased infant anthropometric measurements, with mediating portions ranging from 23.02% to 30.53%. Our findings shed light on the potential mechanisms underlying the effects of prenatal BPs exposure on infant growth and call for urgent actions for risk assessment and regulation of BPF. Future cohort studies with larger sample sizes are warranted to confirm our findings.

01 Jan 2025·Zoological Research

Integrated single-cell transcriptomic map of pig kidney cells across various periods and anatomical sites

Article

Author: Li, Na ; Yao, Tian-Xiong ; Huang, Lu-Sheng

The kidney is essential for maintaining fluid, electrolyte, and metabolite homeostasis, and for regulating blood pressure. The pig serves as a valuable biomedical model for human renal physiology, offering insights across different physiological states. In this study, single-cell RNA sequencing was used to profile 138 469 cells from 12 pig kidney samples collected during the embryonic (E), fattening (F), and pregnancy (P) periods, identifying 29 cell types. Proximal tubule (PT) cells exhibited elevated expression of metabolism-related transcription factors (TFs), including GPD1, ACAA1, and AGMAT, with validation across multiple individuals, periods, and species. Fluorescence homologous double-labeling of paraffin sections further confirmed the expression of ACAA1 and AGMAT in PT cells. Comparative analysis of pig and human kidneys revealed a high degree of similarity among corresponding cell types. Analysis of cell-type heterogeneity highlighted the diversity of thick ascending limb (TAL) cells, identifying a TAL subpopulation related to immune function. Additionally, the functional heterogeneity of kidney-resident macrophages (KRM) was explored across different anatomical sites. In the renal medulla, KRM were implicated in phagocytosis and leukocyte activation, whereas in the renal pelvis, they functioned as ligands, recruiting neutrophils with bactericidal activity to the renal pelvis to combat urinary tract infections.

01 Oct 2024·Science of The Total Environment

Gestational organophosphate esters (OPEs) exposure in association with placental DNA methylation levels of peroxisome proliferator-activated receptors (PPARs) signaling pathway-related genes

Article

Author: Wang, Ziliang ; Song, Shujuan ; Song, Xiuxia ; Miao, Maohua ; Zhu, Haijun ; Wu, Qihan ; Yuan, Wei ; Huang, Baoqin ; Ji, Honglei ; Liang, Hong ; Chen, Yafei

BACKGROUNDOrganophosphate esters (OPEs) exposure could affect offspring health. However, the underlying mechanisms are not well documented.OBJECTIVESBased on a birth cohort study, we aimed to investigate the associations among gestational OPEs exposure, placental DNA methylation levels of peroxisome proliferator-activated receptor (PPAR) signaling pathway-related genes, and fetal growth.METHODSWe measured the concentrations of eight OPE metabolites in maternal urine samples and neonatal anthropometric measurements in 733 mother-child pairs. In 327 placental samples, we assessed the DNA methylation levels of 14 genes which were involved in the PPARs signaling pathway and expressed in placenta. Multiple linear regression models were used to examine the associations of OPEs exposure with placental DNA methylation, and of OPEs and placental DNA methylation with neonatal anthropometric measurements. Causal mediation analyses were conducted to examine the potential mediating role of placental DNA methylation in the pathway between OPEs exposure and fetal growth.RESULTSWe observed a general pattern of OPEs exposure being associated with hypermethylation of candidate genes, with statistically significant associations identified for several OPEs with RXRA, ACAA1, ACADL, ACADM, PLTP, and NR1H3 methylation. Further, gestational exposure to BCIPP, DPP, BBOEP, ∑NCl-OPEs, and ∑OPEs tended to be associated with lower anthropometric measurements, with more significant associations observed on arm circumference, and abdominal and back skinfold thickness. Notably, RXRA, ACAA1, ACOX1, CPT2, ACADM, and NR1H3 methylation tended to be associated with lower neonatal anthropometric measurements, especially for abdominal and back skinfold thickness. Moreover, mediation analyses showed that 19.42 % of the total effect of DPP on the back skinfold thickness was mediated by changes in RXRA methylation, and there was a significant indirect effect of RXRA methylation.CONCLUSIONSGestational OPEs exposure could disrupt the placental DNA methylation levels of PPAR signaling pathway-related genes, which might contribute to the effect of OPEs on fetal growth.

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