نتایج جستجو برای: tubular differentiation

تعداد نتایج: 253331  

2012
Ruth E. Schietke Thomas Hackenbeck Maxine Tran Regina Günther Bernd Klanke Christina L. Warnecke Karl X. Knaup Deepa Shukla Christian Rosenberger Robert Koesters Sebastian Bachmann Peter Betz Gunnar Schley Johannes Schödel Carsten Willam Thomas Winkler Kerstin Amann Kai-Uwe Eckardt Patrick Maxwell Michael S. Wiesener

The Hypoxia-inducible transcription Factor (HIF) represents an important adaptive mechanism under hypoxia, whereas sustained activation may also have deleterious effects. HIF activity is determined by the oxygen regulated α-subunits HIF-1α or HIF-2α. Both are regulated by oxygen dependent degradation, which is controlled by the tumor suppressor "von Hippel-Lindau" (VHL), the gatekeeper of renal...

Journal: :Frontiers in bioscience : a journal and virtual library 2008
Franca Anglani Monica Ceol Federica Mezzabotta Rossella Torregrossa Emilia Tiralongo Enrica Tosetto Dorella Del Prete Angela D'Angelo

The adult mammalian renal tubular epithelium exists in a relatively quiescent to slowly replicating state, but has great potential for regenerative morphogenesis following severe ischemic or toxic injury. Kidney regeneration and repair occur through three cellular and molecular mechanisms: differentiation of the somatic stem cells, recruitment of circulating stem cells and, more importantly, pr...

Journal: :Folia histochemica et cytobiologica 2014
Bernhard Maria Walther Ina Walther Yuan Chen Iver Petersen

GNAS1 codes for a part of the a-stimulatory subunit (Gsa) of the G protein. Mutation of GNAS1 has been frequently found in myxoid soft tissues, however, in gastrointestinal tumors, little is known about the mutation status of GNAS1. The aim of the study was to analyze the occurrence of GNAS1 mutations indifferent gastrointestinal, gastroenteropancreatic neuroendocrine tumors (GEP-NETs) and colo...

Journal: :Clinical science 2000
N Kumagai C N Inoue Y Kondo K Iinuma

Focal tubular cell multiplication at sites on an injured nephron is a critical event in the recovery phase following acute tubular necrosis. During this process, numerous viable tubular cells exfoliate and are shed into the urine. Lysophosphatidic acid (LPA) is generated in the plasma membrane of injured cells and acts as an intercellular mediator of various biological processes, including infl...

Journal: :Kidney international 2006
M Simons G Walz

Polycystic kidneys are caused by an amazingly broad array of genetic mutations and manipulations. The ciliary hypothesis has evolved as the unifying concept of cystogenesis: cilia, bend by fluid flow, initiate a calcium influx that prevents cyst formation. The integrity of ciliary functions has been linked to the polycystic kidney disease gene products localizing to the cilium or the basal body...

Journal: :Journal of cell science. Supplement 1993
E D Avner

Renal cysts are central pathological features in a number of human congenital and acquired diseases, and produce significant morbidity and mortality. This review describes our laboratory's efforts to identify specific alterations in epithelial cell polarity and differentiation associated with renal tubular cyst formation and progressive enlargement. Studies in a murine model of human autosomal ...

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