Podocyte-Specific Deletion of Myh9 Encoding Nonmuscle Myosin Heavy Chain 2A Predisposes Mice to Glomerulopathy
- D. Johnstone, Jidong Zhang, L. Holzman
- Biology, MedicineMolecular and Cellular Biology
- 14 March 2011
Evidence that MYH9 dysfunction in humans results in similar susceptibility to experimental doxorubicin hydrochloride glomerulopathy is reviewed and placed in the context of recent findings in human kidney disease, including the role of APOL1.
Actin-depolymerizing Factor Cofilin-1 Is Necessary in Maintaining Mature Podocyte Architecture*
- P. Garg, R. Verma, L. Holzman
- BiologyJournal of Biological Chemistry
- 15 May 2010
It is concluded that cofilin-1 is necessary for maintenance of normal podocyte architecture and for actin structural changes that occur during induction and recovery from podocyte injury.
Crk1/2-dependent signaling is necessary for podocyte foot process spreading in mouse models of glomerular disease.
- B. George, R. Verma, L. Holzman
- BiologyJournal of Clinical Investigation
- 1 February 2012
The present studies suggest that activation of a Cas-Crk1/2-dependent complex is necessary for foot process effacement observed in distinct subsets of human glomerular diseases.
Motor Protein Myo1c Is a Podocyte Protein That Facilitates the Transport of Slit Diaphragm Protein Neph1 to the Podocyte Membrane
- E. Arif, M. Wagner, D. Nihalani
- BiologyMolecular and Cellular Biology
- 14 March 2011
A novel Myo1c-dependent molecular mechanism is identified that mediates the dynamic organization of Neph1 and nephrin at the slit diaphragm and is critical for podocyte function.
mTOR regulates expression of slit diaphragm proteins and cytoskeleton structure in podocytes.
- B. Vollenbröker, B. George, M. Wolfgart, M. Saleem, H. Pavenstädt, T. Weide
- Biology, MedicineAJP - Renal Physiology
- 1 February 2009
The data provide new molecular insights explaining which pathways and molecules are affected in podocytes by an imbalanced mTOR function because of rapamycin treatment, and reduce cell adhesion and cell motility, which was accompanied by an enhanced formation of dot-like actin-rich structures.
Crk1/2 and CrkL form a hetero-oligomer and functionally complement each other during podocyte morphogenesis
- B. George, Q. Fan, L. Holzman
- BiologyKidney International
- 5 February 2014
Crk1/2 and CrkL are physically-linked, functionally complement each other during podocyte foot process spreading, and together are required for developing typical foot process architecture.
GSK3β inactivation in podocytes results in decreased phosphorylation of p70S6K accompanied by cytoskeletal rearrangements and inhibited motility.
- B. George, B. Vollenbröker, M. Saleem, T. Huber, H. Pavenstädt, T. Weide
- BiologyAJP - Renal Physiology
- 1 May 2011
It is found that prolonged rapamycin treatment in podocytes leads to an increase in glycogen synthase kinase 3β (GSK3β) phosphorylation, resulting in inactivation of total GSK3β kinase activity, suggesting that G SK3 kinase can modulate Akt/mTOR-dependent signaling in Podocytes.
Signaling from the podocyte intercellular junction to the actin cytoskeleton.
- B. George, L. Holzman
- BiologySeminars in Nephrology
- 1 July 2012
Pals1 Haploinsufficiency Results in Proteinuria and Cyst Formation.
- T. Weide, B. Vollenbröker, H. Pavenstädt
- Biology, MedicineJournal of the American Society of Nephrology
- 1 July 2017
Findings support a link between apical polarity proteins and renal diseases, especially renal cyst diseases, and further investigation of the Pals1-linked networks is required to decipher the mechanisms underlying the pathogenesis of these diseases.
Tropomyosin‐related kinase C (TrkC) enhances podocyte migration by ERK‐mediated WAVE2 activation
- Sascha Gromnitza, Carolin Lepa, T. Weide, A. Schwab, H. Pavenstädt, B. George
- BiologyThe FASEB Journal
- 21 November 2017
It is found that the Src homologous and collagen‐like (Shc) binding site Tyr516 within the TrkC cytoplasmic domain was necessary for TrkK‐induced migration of podocytes, which enhances podocyte migration by ERK‐mediated WAVE2 activation.
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