Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Ablation of proximal tubular suppressor of cytokine signaling 3 enhances tubular cell cycling and modifies macrophage phenotype during acute kidney injury.

Kidney international - 1 Jun 2014

Susnik Nathan, Sörensen-Zender Inga, Rong Song, von Vietinghoff Sibylle, Lu Xia, Rubera Isabelle, Tauc Michel, Falk Christine S, Alexander Warren S, Melk Anette, Haller Herrmann, Schmitt Roland

Abstract excerpt

Suppressor of cytokine signaling 3 (SOCS-3) is an important intracellular negative regulator of several signaling pathways. We found that SOCS-3 is highly expressed in renal proximal tubules during acute kidney injury. To test the impact of this, conditional proximal tubular knockout mice (SOCS-3(sglt2Δ/sglt2Δ)) were created. These mice had better kidney function than their wild-type counterparts in aristolochic...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Acute Kidney Injury
Share to Antigens, Differentiation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Janus Kinases

Share to Kidney Tubules, Proximal

Share to Macrophage Activation

Share to STAT Transcription Factors

Share to Suppressor of Cytokine Signaling 3 Protein

Share to Suppressor of Cytokine Signaling Proteins

Source

Identifiers

PMID: 24402091
DOI: 10.1038/ki.2013.525

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Ablation of proximal tubular suppressor of cytokine signaling 3 enhances tubular cell cycling and modifies macrophage phenotype during acute kidney injury.PMID 24402091Read ↗

Loss of activator of G-protein signaling 3 impairs renal tubular regeneration following acute kidney injury in rodents.Semantic proximity Read ↗

Novel insights into STAT3 in renal diseasesSemantic proximity Read ↗

Deletion of STAT3 from Foxd1 cell population protects mice from kidney fibrosis by inhibiting pericytes trans-differentiation and migrationSemantic proximity Read ↗

Innate Immune Signaling Contributes to Tubular Cell Senescence in the Glis2 Knockout Mouse Model of NephronophthisisSemantic proximity Read ↗

Targeting Stat3 with conditional knockout or PROTAC technology alleviates renal injury by Limiting pyroptosisSemantic proximity Read ↗

Sav1 Loss Induces Senescence and Stat3 Activation Coinciding with Tubulointerstitial Fibrosis.Semantic proximity Read ↗

Tubular STAT3 limits renal inflammation in autosomal dominant polycystic kidney diseaseSemantic proximity Read ↗

Mechanism of chronic aristolochic acid nephropathy: role of Smad3Semantic proximity Read ↗

Smad3 deficiency attenuates renal fibrosis, inflammation,and apoptosis after unilateral ureteral obstruction.Semantic proximity Read ↗

Loss of Glis2/NPHP7 causes kidney epithelial cell senescence and suppresses cyst growth in the Kif3a mouse model of cystic kidney disease.Semantic proximity Read ↗

Hepatocyte growth control by SOCS1 and SOCS3Semantic proximity Read ↗

STAT3 inhibition attenuates the progressive phenotypes of Alport syndrome mouse model.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.