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The differential role of Jak/STAT signaling in retinal degeneration

Lange, C; Thiersch, M; Samardzija, M; Grimm, C (2010). The differential role of Jak/STAT signaling in retinal degeneration. In: Anderson, R E; LaVail, M M; Hollyfield, J G. Retinal Degenerative Diseases : Laboratory and Therapeutic Investigations. New York, NY: Springer, 601-607.

Abstract

Retinal degenerative diseases are a major cause of severe visual impairment or blindness in humans. To develop therapeutic strategies it is of particular importance to understand the molecular mechanisms taking place during the progression of the disease. Genes and proteins of the Janus kinase/Signal Transducer and Activator of Transcription (Jak/STAT) signaling pathway have been shown to play an important role in models of retinal degeneration (RD). Here we investigated the expression of additional genes involved in the Jak/STAT pathway in an induced (light exposure) and an inherited (rd1 mouse) model of RD. We show that STAT mRNAs as well as the Jak2/shp-1 pathway are differentially regulated in the two models. In contrast, we show that Jak3 mRNA is upregulated in both, the light damaged and the degenerative retina of the rd1 mouse. This common answer to probably different apoptotic stimuli suggests a prominent role for Jak3 in the damaged retina and could therefore be interesting for further investigations.

Additional indexing

Item Type:Book Section, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Ophthalmology Clinic
04 Faculty of Medicine > Zurich Center for Integrative Human Physiology (ZIHP)
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Life Sciences > General Biochemistry, Genetics and Molecular Biology
Language:English
Date:17 March 2010
Deposited On:05 Jul 2010 15:26
Last Modified:04 Dec 2024 02:38
Publisher:Springer
Series Name:Advances in Experimental Medicine and Biology
Number:664
ISSN:0065-2598
ISBN:978-1-4419-1398-2
Funders:Swiss National Science Foundation (SNF)
OA Status:Closed
Publisher DOI:https://doi.org/10.1007/978-1-4419-1399-9_69
Related URLs:https://link.springer.com/book/10.1007/978-1-4419-1399-9
PubMed ID:20238064
Other Identification Number:978-1-4419-1399-9 (E)
Project Information:
  • Funder: SNSF
  • Grant ID:
  • Project Title: Swiss National Science Foundation (SNF)

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