相关实验视频

Updated: Jul 13, 2025

Identification of Nucleolar Factors During HIV-1 Replication Through Rev Immunoprecipitation and Mass Spectrometry

Identification of Nucleolar Factors During HIV-1 Replication Through Rev Immunoprecipitation and Mass Spectrometry

Published on: June 26, 2019

乙型肝炎病毒核心蛋白稳定RANGAP1以调节KDM2A并促进肝癌发生

Hong-Juan You¹, Li-Hong Ma¹, Xing Wang¹

¹Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Medical University, Xuzhou, Jiangsu, China.

Cellular oncology (Dordrecht, Netherlands)

|October 16, 2023

概括

乙型肝炎病毒核心蛋白 (HBC) 通过与RANGAP1和KDM2A相互作用促进肝癌. 这些蛋白质增强瘤生长和迁移,为HBV相关的恶性瘤提供潜在的治疗点.

科学领域:

肝病学肝病学是一种肝病学.
在瘤学瘤学.
分子生物学分子生物学

背景情况:

乙型肝炎病毒核心蛋白 (HBC) 是HBV核体的组成部分,并与肝癌发生有关.
了解HBC诱导瘤发生的分子机制对于开发向疗法至关重要.

研究的目的:

研究RANGAP1和KDM2A在HBC介导的瘤发生中的作用.
阐明肝细胞癌 (HCC) 中HBC,RANGAP1和KDM2A之间的相互作用网络.

主要方法:

同免疫沉 (Co-IP) 和质谱测量用于识别与HBC相互作用的蛋白质.
在HCC组织中对RANGAP1和KDM2A表达的定量分析.
在体外和体内研究,以评估RANGAP1和KDM2A在HCC细胞中的功能作用.
西方斑点用于确认蛋白质相互作用和稳定.

主要成果:

HBC与RANGAP1和KDM2A相互作用,这两者都在HCC组织中升级调节.
通过增强RANGAP1和KDM2A稳定,HBC促进HCC细胞的生长和迁移.
HBC破坏了RANGAP1和KDM2A与E3结合酶SYVN1的相互作用,导致它们的稳定性增加.
通过RANGAP1,RANGAP1促进KDM2A的稳定,而HBC则通过RANGAP1对KDM2A的表达进行上调.

结论:

HBC通过一种涉及RANGAP1和KDM2A的新机制促进肝癌发生.
RANGAP1和KDM2A代表了治疗HBV相关肝癌的潜在分子标.

关键词:

在HBC中,HBC就是HBC.肝细胞癌是肝细胞癌.这就是KDM2A.兰加普 (RANGAP) 是一个这就是SYVN1的意思.

更多相关视频

Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle

Development of a Hepatitis B Virus Reporter System to Monitor the Early Stages of the Replication Cycle

Published on: February 1, 2017

Studying RNA Interactors of Protein Kinase RNA-Activated during the Mammalian Cell Cycle

Studying RNA Interactors of Protein Kinase RNA-Activated during the Mammalian Cell Cycle

Published on: March 5, 2019

相关概念视频

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...

Abnormal Proliferation

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...

mTOR Signaling and Cancer Progression

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...

The Ras Gene

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...

MAPK Signaling Cascades

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...

Mechanisms of Retrovirus-induced Cancers

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...