Video Experimental Relacionado

Updated: Feb 28, 2026

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Published on: January 7, 2013

DUSP26 protege contra la lesión renal aguda al desfosforilar p53 en la serina 312

Ying Fu^1,2,3, Yu Xiang¹, Yun Han¹

¹Department of Nephrology, Hunan Key Laboratory of Kidney Disease and Blood Purification, Institute of Nephrology, The Second Xiangya Hospital at Central South University, Changsha, China.

Nature communications

|February 26, 2026

Abstract:

Acute kidney injury (AKI) remains a leading cause of morbidity and mortality, yet the molecular pathways driving kidney tubule damage in AKI are not fully understood. Here, we report dual-specificity phosphatase 26 (DUSP26) as a critical regulator of kidney tubule injury in AKI. In our study, DUSP26 expression was markedly reduced in kidney biopsies from AKI patients of both sexes and in male murine models of cisplatin nephrotoxic and ischemic AKI. This down-regulation was driven by hypermethylation of the gene promoter of DUSP26 in kidney tubular cells. Loss of DUSP26 exacerbated tubular damage, whereas knock-in of DUSP26 specifically in kidney proximal tubule cells conferred protection. Mechanistically, DUSP26 directly bound to p53 to dephosphorylate it at serine 312, dampening the transcriptional activity of p53 towards cell death genes. Pharmacologic inhibition of DUSP26 sensitized kidneys to AKI, whereas DUSP26 overexpression was protective. Pharmacologic inhibition of DUSP26 also exacerbated ischemia-reperfusion injury in the liver. These findings uncover DUSP26 as a key phosphatase guarding against tissue injury by dephosphorylating p53 at serine 312, and highlight the DUSP26-p53 axis as a promising therapeutic target.

Palabras clave:

lesión renal aguda DUSP26 p53 fosfatasa de doble especificidad apoptosis nefrología biología molecular bioquímica

Más Videos Relacionados

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection

Published on: November 10, 2021

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

Videos de Conceptos Relacionados

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...

DNA Damage Can Stall the Cell Cycle

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

DNA Damage can Stall the Cell Cycle

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

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...

Acute Kidney Injury II: Pathophysiology

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...

The JAK-STAT Signaling Pathway

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...