预约演示

更新于：2025-05-07

ABCB5

更新于：2025-05-07

基本信息

别名

ABCB5、ABCB5 P-gp、ABCB5alpha

+ [7]

简介

Energy-dependent efflux transporter responsible for decreased drug accumulation in multidrug-resistant cells (PubMed:12960149, PubMed:15205344, PubMed:15899824, PubMed:22306008). Specifically present in limbal stem cells, where it plays a key role in corneal development and repair (By similarity).

关联

项与 ABCB5 相关的药物

CN115260098

专利挖掘

靶点

ABCB5

作用机制

ABCB5 inhibitors

在研机构

澳门科技大学

原研机构

澳门科技大学

在研适应症

类风湿关节炎

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 ABCB5 相关的临床结果

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100 项与 ABCB5 相关的转化医学

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0 项与 ABCB5 相关的专利（医药）

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778

项与 ABCB5 相关的文献（医药）

2025-04-22·Proceedings of the National Academy of Sciences

Functional redundancy in the toxic pathway of Bt protein Cry1Ab, but not Cry1Fa, against the Asian corn borer

Article

作者: Wang, Xingliang ; Yang, Yihua ; Zhai, Yuqian ; Zhuang, Xuna ; Wu, Shuwen ; Yue, Yujin ; Wu, Yidong ; Tabashnik, Bruce E. ; Wang, Falong

Crops genetically engineered to produce insecticidal proteins from the bacterium Bacillus thuringiensis (Bt) have been used extensively to control some major crop pests, but their benefits decrease when pests evolve resistance. Better understanding of the genetic basis of resistance is needed to effectively monitor, manage, and counter pest resistance to Bt crops. Resistance to Bt proteins in at least 11 species of Lepidoptera, including many important crop pests, is associated with naturally occurring mutations that disrupt one or more of three larval midgut proteins: cadherin and ATP-binding cassette proteins ABCC2 and ABCC3. Here, we determined how CRISPR/Cas9-mediated mutations disrupting cadherin, ABCC2, and ABCC3 singly and in pairs affect resistance to Bt proteins Cry1Ab and Cry1Fa in the Asian corn borer ( Ostrinia furnacalis ), which is the most damaging pest of corn in Asia and is closely related to the European corn borer ( Ostrinia nubilalis ), a major pest in Europe and North America. The results from bioassays of six knockout strains and their parent susceptible strain support a model in which Cry1Ab can kill larvae via one path requiring ABCC2 or another path requiring cadherin and ABCC3, whereas Cry1Fa uses only the first path. The model’s predictions are generally supported by results from genetic linkage analyses and responses to Cry1Ab and Cry1Fa of Sf9 cells and Xenopus oocytes modified to produce cadherin, ABCC2, and ABCC3 singly or in pairs. The functional redundancy identified here for Cry1Ab could sustain its efficacy against O. furnacalis and may exemplify a widespread natural strategy for delaying resistance.

2025-03-01·Journal of Clinical Laboratory Analysis

Integrated Analysis of WES and scRNA‐Seq Data Reveals the Genetic Basis of Immune Dysregulation in Unexplained Recurrent Pregnancy Loss

Article

作者: Guo, Shuai ; Lin, Zhao‐Jing ; Zhi, Ya‐Nan ; Li, Ya‐Li ; Liu, Shu ; Zhu, Lei ; Fan, Liang‐Liang ; Jiang, Yu‐Jie ; Dong, Yi ; Sun, Yan‐Mei ; Zhang, Wei ; Yun, Jiao

ABSTRACTObjectiveThis study aimed to identify genetic variants and their functional consequences underlying Unexplained Recurrent Pregnancy Loss (uRPL) through comprehensive genomic and transcriptomic analyses.MethodsWe recruited 13 Chinese uRPL patients and performed Whole Exome Sequencing (WES) on chorionic villi samples from miscarriage tissues. Additionally, we conducted an integrative analysis using single‐cell RNA sequencing data from decidual immune cells to examine expression patterns.ResultsWES analysis pinpointed variants in the four MUC genes (MUC4, MUC6, MUC16, and MUC17), six lipid metabolism genes in immune cells (ABCA4, ABCA7, ABCB5, ABCC8, ADGRV1, and ANK3), and two structural genes (PIEZO1 and PKD1), whose variants impair mucosal barriers and lipid homeostasis, thereby leading to immune dysregulation and contributing to uRPL. To delve deeper into the effects of these genetic variants on cellular expression patterns, we undertook an integrative analysis using a single‐cell dataset from decidual immune cells in uRPL cases. We observed significant dysregulation of lipid metabolism within immune cells, reduced heat shock protein expression, and enhanced chemokine signaling in uRPL samples, indicating a pro‐inflammatory state.ConclusionsIn summary, our study reveals a complex interplay between genetic variants and immune cell dysfunctions in uRPL, emphasizing the role of identified genetic variants in driving pro‐inflammatory states. These findings provide a comprehensive view of the molecular mechanisms underlying uRPL, opening paths for novel therapeutic interventions and improved clinical management.

2025-01-01·Cellular Signalling

The BET inhibitor JQ1 suppresses tumor survival by ABCB5-mediated autophagy in uveal melanoma

Article

作者: Cheng, Yaqi ; Chen, Minghao ; Wang, Zhichong ; Gu, Simin ; Chen, Shuxia ; Cui, Zedu ; Liu, Weiqin ; Sang, Xuan ; Su, Yaru ; Liu, Chang ; Wang, Xiaoran ; Wan, Qi ; Liu, Ying ; Li, Chaoyang

Uveal melanoma (UM), the most common adult ocular tumor, is aggressive and resistant to treatment, posing threat to patients' lives. The novel, effective therapies and the exploration of chemosensitizer for UM are imperative. The anticancer efficacy was evaluated with and without JQ1 treatment or ABCB5 gene silencing or overexpression. RNA sequencing identified downstream effectors in JQ1-treated cells. Integrated analysis of The Cancer Genome Atlas data (TCGA) and immunohistochemistry (IHC) revealed the oncogenic role of ABCB5. Functional analyses of JQ1 and defective ABCB5 were conducted using flow cytometry, transmission electron microscopy (TEM), IHC and western blot. The effects of JQ1 were validated in a heterotopic tumor model derived from OCM-1 cells. JQ1 inhibited cell proliferation, migration and invasion, induced cell cycle arrest and promoted apoptosis. JQ1 also suppressed the survival of UM in heterotopic tumor model. RNA sequencing indicated that JQ1 down-regulated the expressions of ABCB5 and autophagy-related genes, which was confirmed in vitro and in vivo by western blot. ABCB5, a marker associated with cancer stem cells and chemo-resistance, exhibited heightened expression in UM tissues, linked to immune infiltration. Notably, disrupting ABCB5 expression impeded UM cell proliferation and interfered with autophagy. Moreover, the overexpression of ABCB5 promoted cell proliferation, migration and invasion, and rescued autophagy related gene expression. Of note, JQ1 enhanced the sensitivity of OCM-1 cells to chemotherapy. Thus JQ1 inhibits UM survival via ABCB5-mediated autophagy and enhances chemo-sensitivity, suggesting potential for BET-based approaches in UM clinical management.

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