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Last update 08 May 2025

RNF152

Last update 08 May 2025

Basic Info

Synonyms

E3 ubiquitin-protein ligase RNF152, FLJ39176, ring finger protein 152

+ [2]

Introduction

E3 ubiquitin-protein ligase that acts as a negative regulator of mTORC1 signaling by mediating ubiquitination of RagA/RRAGA and RHEB (PubMed:25936802, PubMed:30514904). Catalyzes 'Lys-63'-linked polyubiquitination of RagA/RRAGA in response to amino acid starvation, thereby regulating mTORC1 signaling (PubMed:25936802). Also mediates monoubiquitination of RHEB, promoting its association with the TSC-TBC complex and subsequent inhibition (PubMed:30514904). Also mediates 'Lys-48'-linked polyubiquitination of target proteins and their subsequent targeting to the proteasome for degradation (PubMed:21203937). Induces apoptosis when overexpressed (PubMed:21203937).

Drugs associated with RNF152

KRAS G12D LYMTAC (Amgen)

Target

KRAS G12D x RNF152

Mechanism

KRAS G12D inhibitors [+1]

Active Org.

Amgen, Inc.

Originator Org.

Amgen, Inc.

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with RNF152

100 Translational Medicine associated with RNF152

0 Patents (Medical) associated with RNF152

Literatures (Medical) associated with RNF152

02 Sep 2024·British Poultry Science

Molecular and transcriptomic analysis of the ovary during laying and brooding stages in Zhedong white geese ( Anser cygnoides domesticus )

Article

Author: Zang, Z ; Liu, G ; Li, B ; Wang, S ; Wang, Y ; Huang, H ; Zhao, X

1. This study investigates the molecular mechanisms affecting brooding in Zhedong white geese by examining differences in reproductive endocrine levels, ovarian histology and transcriptomics.2. Twenty 18-month-old Zhedong white geese were selected to examine their ovaries using histological, biochemical, molecular biological, and high-throughput sequencing techniques during the laying and brooding periods.3. The results showed that the number of atretic follicles and apoptotic cells in the ovaries increased significantly (p < 0.05), the levels of follicle-stimulating hormone, luteinising hormone, gonadotropin-releasing hormone and oestradiol decreased significantly (p < 0.05), and the level of prolactin increased significantly (p < 0.01) during the brooding stage.4. In broody geese, the expression of CASP3, CASP9, P53, BAX, and Cyt-c were considerably higher (p < 0.05), but BCL2 expression was significantly lower (p < 0.05).5. In ovarian tissues, 260 differentially expressed lncRNAs, 13 differentially expressed miRNA and 60 differentially expressed mRNA were all discovered using transcriptome sequencing analysis. Functional enrichment analysis revealed that the differentially expressed mRNA and non-coding RNA target genes were primarily involved in ECM-receptor interaction, cell adhesion, cardiac muscle contraction, mTOR signalling, and the calcium signalling pathway.6. In conclusion, follicular atrophy and apoptosis occurred in the ovaries and serum reproductive hormone levels were significantly changed during the brooding period of Zhedong white geese. COL3A1, COL1A2, GRIA1, RNF152, miR-192, and miR-194 may be important candidates for the regulation of brooding behaviour, with the mTOR signalling pathway playing a key role.

01 May 2024·iScience

Fasting-induced RNF152 resensitizes gallbladder cancer cells to gemcitabine by inhibiting mTORC1-mediated glycolysis

Article

Author: Shen, Sheng ; Zan, Rui ; Sun, Wentao ; Lu, Xiao ; Liu, Han ; Shu, Mengxuan ; Ding, Yaqi ; Tao, Ying ; Gong, Zijun ; Liu, Houbao ; Zheng, Bohao ; Ma, Chaolin ; Ni, Xiaoling ; Suo, Tao

Abnormal mTORC1 activation by the lysosomal Ragulator complex has been implicated in cancer and glycolytic metabolism associated with drug resistance. Fasting upregulates RNF152 and mediates the metabolic status of cells. We report that RNF152 regulates mTORC1 signaling by targeting a Ragulator subunit, p18, and attenuates gemcitabine resistance in gallbladder cancer (GBC). We detected levels of RNF152 and p18 in tissues and undertook mechanistic studies using activators, inhibitors, and lentivirus transfections. RNF152 levels were significantly lower in GBC than in adjacent non-cancer tissues. Fasting impairs glycolysis, induces gemcitabine sensitivity, and upregulates RNF152 expression. RNF152 overexpression increases the sensitivity of GBC cells to gemcitabine, whereas silencing RNF152 has the opposite effect. Fasting-induced RNF152 ubiquitinates p18, resulting in proteasomal degradation. RNF152 deficiency increases the lysosomal localization of p18 and increases mTORC1 activity, to promote glycolysis and decrease gemcitabine sensitivity. RNF152 suppresses mTORC1 activity to inhibit glycolysis and enhance gemcitabine sensitivity in GBC.

01 Oct 2023·The American Journal of Pathology

RNF152 Suppresses Fatty Acid Oxidation and Metastasis of Lung Adenocarcinoma by Inhibiting IRAK1-Mediated AKR1B10 Expression

Article

Author: Zhao, Yang ; Yang, Zhichang ; Yang, Yang ; Zhu, Dengyan ; Nie, Yunfei ; Chen, Xiaoming

Lung adenocarcinoma (LUAD) is a common subtype of primary lung cancer. Fatty acid oxidation plays a key role in LUAD development by providing energy for tumor cells. This study aimed to identify the role of ring finger protein 152 (RNF152) in LUAD. RNF152 was down-regulated in LUAD, and low RNF152 expression correlated with a poor prognosis in LUAD patients. RNF152 overexpression inhibited the proliferation and malignant phenotype of LUAD cells, whereas RNF152 knockdown exerted an opposite effect. Tumor cells overexpressing RNF152 showed less fatty acid oxidation compared with control cells, whereas RNF152 knockdown induced fatty acid uptake and oxidation. Further analysis revealed the binding reaction between RNF152 and interleukin-1 receptor-associated kinase 1 (IRAK1). RNF152 reduced the stability of IRAK1 in LUAD cells by promoting its ubiquitination. RNF152-overexpressed tumor cells exhibited a significantly lower level of Aldo-Keto reductase family 1 member 10 (AKR1B10), whereas up-regulation of IRAK1 restored the expression of AKR1B10 in RNF152-overexpressed cells. Furthermore, up-regulation of IRAK1 eliminated the antitumor effect of RNF152 in LUAD cells. Mouse xenograft models confirmed the inhibitory effect of RNF152 on the tumorigenesis and metastasis of LUAD. Taken together, RNF152 played a tumor suppressive role in LUAD by promoting IRAK1 ubiquitination and IRAK1-mediated down-regulation of AKR1B10, thereby reversing the malignant phenotype of LUAD.

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RNF152

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