Cyclin G1 and TASCC regulate kidney epithelial cell G 2 -M arrest and fibrotic maladaptive repair

Author:

Canaud Guillaume123,Brooks Craig R.14ORCID,Kishi Seiji15ORCID,Taguchi Kensei4ORCID,Nishimura Kenji5,Magassa Sato2,Scott Adam16ORCID,Hsiao Li-Li1ORCID,Ichimura Takaharu1ORCID,Terzi Fabiola2,Yang Li7,Bonventre Joseph V.189ORCID

Affiliation:

1. Renal Division, Brigham and Women’s Hospital, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.

2. INSERM U1151, Institut Necker-Enfants Malades, Université Paris Descartes, Paris 75743, France.

3. Service de Néphrologie et Transplantation Adultes, Hôpital Necker-Enfants Malades, Paris 75743, France.

4. Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA.

5. Department of Nephrology, Graduate School of Biomedical Sciences, Tokushima University, Tokushima 7708503, Japan.

6. Division of Nephrology, Department of Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.

7. Renal Division, Peking University First Hospital, Beijing 100871, China.

8. Division of Health Sciences and Technology, Harvard–Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

9. Harvard Stem Cell Institute, Cambridge, MA 02138, USA.

Abstract

Cyclin G1 regulates G 2 -M arrest in proximal tubular cells, promoting a TASCC-induced secretory phenotype, fibrosis, and kidney disease progression.

Funder

National Institutes of Health

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

Reference51 articles.

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