KDELR: Beyond protein retrieval, a novel regulator in cancer progression

IF 4.2 2区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-07-21 DOI:10.1016/j.bbadis.2025.167981

Diego Tapia , Felipe Garín-Ortiz , Emilia Flores , Manuel Varas-Godoy , Alejandro Godoy , Jorge Cancino

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引用次数: 0

Abstract

Eukaryotic cells interact with their environment through the secretory pathway, which involves the endoplasmic reticulum (ER), Golgi complex (GC), and endolysosomal system. These organelles regulate protein folding, post-translational modifications, and trafficking of structural and signaling proteins essential for cellular homeostasis. The KDEL receptor (KDELR), a cargo and signaling receptor located in the Golgi complex (GC), plays a crucial role in maintaining the balance of the secretory pathway by sensing cargo arrival from the endoplasmic reticulum (ER) and activating signaling pathways. Dysfunction in this pathway contributes to diseases such as diabetes, neurodegenerative disorders, and cancer. Recent studies highlight KDELR's involvement in cancer progression, yet its precise role remains unclear. This review provides an overview of KDELR's structure and function, highlighting its emerging significance in cancer biology.

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KDELR：超越蛋白质检索，一种新的癌症进展调节因子。

真核细胞通过分泌途径与环境相互作用，包括内质网（ER）、高尔基复合体（GC）和内溶酶体系统。这些细胞器调节蛋白质折叠，翻译后修饰，以及细胞稳态所必需的结构和信号蛋白的运输。KDEL受体（KDELR）是位于高尔基复合体（GC）中的一种货物和信号受体，通过感知来自内质网（ER）的货物到达并激活信号通路，在维持分泌途径的平衡中起着至关重要的作用。这条通路的功能障碍会导致糖尿病、神经退行性疾病和癌症等疾病。最近的研究强调KDELR与癌症进展有关，但其确切作用尚不清楚。本文综述了KDELR的结构和功能，并强调了其在癌症生物学中的重要意义。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Biochimica et biophysica acta. Molecular basis of disease 生物-生化与分子生物学

CiteScore

12.30

自引率

0.00%

发文量

218

审稿时长

32 days

期刊介绍： BBA Molecular Basis of Disease addresses the biochemistry and molecular genetics of disease processes and models of human disease. This journal covers aspects of aging, cancer, metabolic-, neurological-, and immunological-based disease. Manuscripts focused on using animal models to elucidate biochemical and mechanistic insight in each of these conditions, are particularly encouraged. Manuscripts should emphasize the underlying mechanisms of disease pathways and provide novel contributions to the understanding and/or treatment of these disorders. Highly descriptive and method development submissions may be declined without full review. The submission of uninvited reviews to BBA - Molecular Basis of Disease is strongly discouraged, and any such uninvited review should be accompanied by a coverletter outlining the compelling reasons why the review should be considered.