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Emerging biomarkers and potential therapeutics of the BCL-2 protein family: the apoptotic and anti-apoptotic context
Egyptian Journal of Medical Human Genetics Pub Date : 2024-01-27 , DOI: 10.1186/s43042-024-00485-7
Md. Saddam , Shamrat Kumar Paul , Mohammad Ahsan Habib , Md. Abrar Fahim , Afsana Mimi , Saiful Islam , Bristi Paul , Md Mostofa Uddin Helal

Apoptosis, also known as the programmed death of cells, is responsible for maintaining the homeostasis of tissues, and this function is carried out by caspases. The process of apoptosis is carried out via two distinct pathways: the extrinsic pathway, which is governed by death receptors, and the intrinsic pathway, also known as the mitochondrial pathway. The BCL-2 protein family encoded by the BCL-2 gene, located at the 18q21.33 chromosomal location, is in charge of regulating the intrinsic pathway, which is responsible for inducing cell death via the permeabilization of the mitochondrial membrane and the release of apoptosis-inducing components. The BCL-2 homology (BH1, BH2, BH3, BH4) domains of this family proteins are crucial for their functioning, and their common BH domains allow interactions between members of the same family and can also serve as indications of pro- or anti-apoptotic activity. A direct correlation may be shown between the overexpression of BCL-2 and the postponement of cell death. It has been determined that a change in the expression of BCL-2 is the root cause of a variety of malignancies, including lung, breast, melanoma, and chronic lymphocytic leukemia, multiple sclerosis, diabetes. In this review, we addressed the genetic information and structural homology of BCL-2 family members. Further, we elucidate the pro-apoptotic and anti-apoptotic roles of the family members. This review highlights the most recent developments in the BCL-2 protein family and presents evidence that targeting this family proteins may have a positive impact on the treatment of medical problems that are still underserved.

中文翻译:

BCL-2 蛋白家族的新兴生物标志物和潜在疗法:凋亡和抗凋亡背景

细胞凋亡,也称为细胞的程序性死亡,负责维持组织的稳态,这一功能是由半胱天冬酶来执行的。细胞凋亡过程通过两种不同的途径进行:由死亡受体控制的外在途径和内在途径,也称为线粒体途径。BCL-2 基因编码的 BCL-2 蛋白家族位于 18q21.33 染色体位置,负责调节内在途径,通过线粒体膜的透化和释放细胞凋亡诱导成分。该家族蛋白的 BCL-2 同源性(BH1、BH2、BH3、BH4)结构域对其功能至关重要,它们共同的 BH 结构域允许同一家族成员之间的相互作用,也可以作为亲或抗的指示。凋亡活性。BCL-2 的过度表达与细胞死亡的推迟之间可能存在直接相关性。已确定BCL-2表达的变化是多种恶性肿瘤的根本原因,包括肺癌、乳腺癌、黑色素瘤、慢性淋巴细胞白血病、多发性硬化症、糖尿病。在这篇综述中,我们讨论了 BCL-2 家族成员的遗传信息和结构同源性。此外,我们阐明了家族成员的促凋亡和抗凋亡作用。这篇综述重点介绍了 BCL-2 蛋白家族的最新进展,并提供了证据表明针对该家族蛋白可能对治疗仍然服务不足的医疗问题产生积极影响。
更新日期:2024-01-27
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