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Related Concept Videos

The JAK-STAT Signaling Pathway01:20

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...
Abnormal Proliferation02:23

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 daughter...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...

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Related Experiment Video

Updated: May 31, 2026

Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
10:09

Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark

Published on: January 26, 2018

SPARC Drives Tubulointerstitial Fibrosis through Regulating the CBP-DOT1L Pathway.

Huimin Jiang1, Qing Yang1, Kuo Wang1

  • 1Department of Nephrology, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Children and Adolescents' Health and Diseases, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatric Metabolism and Inflammatory Diseases, Chongqing, P.R. China.

International Journal of Biological Sciences
|May 29, 2026
PubMed
Summary
This summary is machine-generated.

SPARC protein drives kidney fibrosis by stabilizing DOT1L, a key epigenetic regulator. Targeting the SPARC-CBP-DOT1L pathway offers a novel therapeutic strategy for chronic kidney disease (CKD).

Keywords:
CBPCKDDOT1LPTECsSPARCtubulointerstitial fibrosis

Related Experiment Videos

Last Updated: May 31, 2026

Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
10:09

Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark

Published on: January 26, 2018

Area of Science:

  • Nephrology
  • Molecular Biology
  • Epigenetics

Background:

  • Renal tubulointerstitial fibrosis (TIF) is a major driver of chronic kidney disease (CKD) progression.
  • Current anti-fibrotic therapies for CKD are limited, necessitating new therapeutic targets.

Purpose of the Study:

  • To identify key mediators of TIF and explore potential therapeutic targets for CKD.

Main Methods:

  • Correlation analysis of SPARC expression in human CKD biopsies and murine models (UUO, IRI).
  • Genetic ablation of Sparc in murine models to assess its role in renal fibrosis.
  • Investigation of the SPARC-CBP-DOT1L signaling axis and its epigenetic modifications (H3K79me2).

Main Results:

  • SPARC expression correlates strongly with fibrosis severity in human and murine kidneys.
  • Genetic deletion of Sparc significantly reduces renal fibrosis in UUO and IRI models.
  • SPARC stabilizes DOT1L via the CBP-MEK-ERK pathway, enhancing H3K79me2 and promoting PTECs fibrosis.

Conclusions:

  • SPARC is a critical mediator of renal tubulointerstitial fibrosis (TIF) in chronic kidney disease (CKD).
  • The SPARC-CBP-DOT1L signaling cascade represents a novel epigenetic pathway driving renal fibrosis.
  • Targeting the SPARC-CBP-DOT1L axis holds promise for developing new anti-fibrotic therapies for CKD.