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Last update 23 Jan 2025

ARID4B

Last update 23 Jan 2025

Basic Info

Synonyms

180 kDa Sin3-associated polypeptide, ARID domain-containing protein 4B, ARID4B

+ [11]

Introduction

Acts as a transcriptional repressor (PubMed:12724404). May function in the assembly and/or enzymatic activity of the Sin3A corepressor complex or in mediating interactions between the complex and other regulatory complexes (PubMed:12724404). Plays a role in the regulation of epigenetic modifications at the PWS/AS imprinting center near the SNRPN promoter, where it might function as part of a complex with RB1 and ARID4A. Involved in spermatogenesis, together with ARID4A, where it functions as a transcriptional coactivator for AR (androgen receptor) and enhances expression of genes required for sperm maturation. Regulates expression of the tight junction protein CLDN3 in the testis, which is important for integrity of the blood-testis barrier. Plays a role in myeloid homeostasis where it regulates the histone methylation state of bone marrow cells and expression of various genes involved in hematopoiesis. May function as a leukemia suppressor (By similarity).

Drugs associated with ARID4B

WO2022232169

Patent Mining

Target

ARID4B

Mechanism-

Active Org.

University of Massachusetts [+1]

Originator Org.

University of Massachusetts [+1]

Active Indication

Nutritional and Metabolic Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ARID4B

100 Translational Medicine associated with ARID4B

0 Patents (Medical) associated with ARID4B

187

Literatures (Medical) associated with ARID4B

01 Mar 2025·Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology

CircArid4b: A novel circular RNA regulating antibacterial response during hypoxic stress via apoptosis in yellow catfish (Pelteobagrus fulvidraco)

Article

Author: Li, Jiayi ; Xin, Yingying ; Sun, Xinxin ; Yin, Shaowu ; Ning, Xianhui ; Zhou, Linxin

The intricate interaction among host, pathogen, and environment significantly influences aquatic health, yet the influence of hypoxic stress combined with bacterial infection on host response is understudied. Circular RNAs with stable closed-loop structures have emerged as important regulators in immunity, yet remain ill-defined in fish. In this study, we systematically explored the circRNA response in yellow catfish subjected to combined hypoxia-bacterial infection (HB) stress. Following HB stress, H&E and TUNEL staining identified heightened hepatocyte apoptosis, intracellular vacuolation, and inflammatory tissue damage. RT-qPCR elucidated that differentially expressed genes stimulated by HB synergistically enhanced apoptosis and inflammatory responses. Importantly, we systematically evaluated differentially expressed circRNAs (DEcirs) in yellow catfish under hypoxia with and without Aeromonas veronii infection and identified a novel HB-specific DEcir, designated as circArid4b, whose parental gene Arid4b is highly associated with apoptosis. Experiments confirmed the circular structure of circArid4b and revealed that under HB stimulation, specific knockdown of circArid4b inhibited the expression of Arid4b, while concurrent alterations in multiple apoptosis- and inflammation-related genes synergistically indicated the promotion of apoptotic and inflammatory pathways. Notably, the downregulation of circArid4b expression significantly reduced the susceptibility to bacterial infection in yellow catfish during hypoxia. These results suggest that HB-induced suppression of circArid4b promotes cell apoptosis and inflammation by inhibiting its parental gene and thereby facilitating resistance to bacterial infection during hypoxia. Our study enriches the understanding of fish circRNA mechanisms and offers novel preventive and control strategies for bacterial infections in fish under hypoxic environments.

01 Jan 2025·Metabolism

Disruption of branched-chain amino acid homeostasis promotes the progression of DKD via enhancing inflammation and fibrosis-associated epithelial-mesenchymal transition

Article

Author: Tang, Chao ; Li, Ting ; Zhang, Xuejiao ; Chen, Liming ; Sun, Haipeng ; Li, Xiaoyu ; Deng, Xiaoqing ; Fang, Ting ; Sun, Bei ; Liu, Yajin

BACKGROUND AND AIMSThe disrupted homeostasis of branched-chain amino acids (BCAAs, including leucine, isoleucine, and valine) has been strongly correlated with diabetes with a potential causal role. However, the relationship between BCAAs and diabetic kidney disease (DKD) remains to be established. Here, we show that the elevated BCAAs from BCAAs homeostatic disruption promote DKD progression unexpectedly as an independent risk factor.METHODS AND RESULTSSimilar to other tissues, the suppressed BCAAs catabolic gene expression and elevated BCAAs abundance were detected in the kidneys of type 2 diabetic mice and individuals with DKD. Genetic and nutritional studies demonstrated that the elevated BCAAs from systemic disruption of BCAAs homeostasis promoted the progression of DKD. Of note, the elevated BCAAs promoted DKD progression without exacerbating diabetes in the animal models of type 2 DKD. Mechanistic studies demonstrated that the elevated BCAAs promoted fibrosis-associated epithelial-mesenchymal transition (EMT) by enhancing the activation of proinflammatory macrophages through mTOR signaling. Furthermore, pharmacological enhancement of systemic BCAAs catabolism using small molecule inhibitor attenuated type 2 DKD. Finally, the elevated BCAAs also promoted DKD progression in type 1 diabetic mice without exacerbating diabetes.CONCLUSIONBCAA homeostatic disruption serves as an independent risk factor for DKD and restoring BCAA homeostasis pharmacologically or dietarily represents a promising therapeutic strategy to ameliorate the progression of DKD.

01 Jan 2025·Biochemical and Biophysical Research Communications

Dephosphorylation of branched-chain α-keto acid dehydrogenase E1α (BCKDHA) promotes branched-chain amino acid catabolism and renders cancer cells resistant to X-rays by mitigating DNA damage

Article

Author: Osaki, Tsukasa ; Fujii, Junichi ; Bo, Tomoki

Branched-chain amino acids (BCAAs) facilitate cancer cell proliferation and survival. Stresses, including X-irradiation, increase BCAA uptake. However, the role of BCAA metabolism in cancer cell survival remains unclear. Therefore, this study aimed to elucidate the role of the BCAA catabolic pathway in cancer cell survival following X-irradiation. X-irradiation dose-dependently dephosphorylated branched-chain α-keto acid dehydrogenaseE1α (BCKDHA) suggesting the activation of the BCKDH complex, which catalyzes the rate-determining step of BCAA catabolism. We considered that activation of BCKDH promoted the BCAA catabolism, which resulted in cancer cell resistance to X-irradiation. Consistent with this notion, cells with BCKDHA knockdown exhibited increased radiosensitivity, which was associated with the increase in mitotic catastrophe and residual double-strand breaks by decreasing cellular ATP levels after X-irradiation. Our results suggest that BCKDHA dephosphorylation promotes BCAA catabolism, leading to cell survival by mitigating DNA damage after X-irradiation. Thus, BCAA catabolic pathway may be a target for radiation therapy.

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ARID4B

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