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Up-regulation and increased phosphorylation of protein kinase C (PKC) delta, mu and theta in the degenerating rd1 mouse retina.

Azadi, Seifollah LU ; Paquet-Durand, Francois LU ; Medstrand, Patrik LU orcid ; van Veen, Theo LU and Ekström, Per LU (2006) In Molecular and Cellular Neuroscience 31(4). p.759-773
Abstract
The rd1 mouse serves as a model for inherited photoreceptor degeneration: retinitis pigmentosa. Microarray techniques were employed to compare the transcriptomes of rd1 and congenic wild-type retinas at postnatal day 11, when degenerative processes have started but most photoreceptors are still present. Of the several genes that were differentially expressed, focus was put on those associated with the protein kinase C (PKC) signaling pathway, in particular PKCδ, μ and θ. Microarray identified these as being up-regulated in the rd1 retina, which was confirmed by QRT-PCR. Western blotting and immunostaining, using antibodies against either total or phosphorylated variants of the PKC isoforms, revealed increased expression and phosphorylation... (More)
The rd1 mouse serves as a model for inherited photoreceptor degeneration: retinitis pigmentosa. Microarray techniques were employed to compare the transcriptomes of rd1 and congenic wild-type retinas at postnatal day 11, when degenerative processes have started but most photoreceptors are still present. Of the several genes that were differentially expressed, focus was put on those associated with the protein kinase C (PKC) signaling pathway, in particular PKCδ, μ and θ. Microarray identified these as being up-regulated in the rd1 retina, which was confirmed by QRT-PCR. Western blotting and immunostaining, using antibodies against either total or phosphorylated variants of the PKC isoforms, revealed increased expression and phosphorylation of PKCδ, μ and θ in the rd1 retina at the protein level as well. Our results suggest that these PKC isoforms are involved in rd1 degeneration. (Less)
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author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Apoptosis, Kinase, Microarray, Photoreceptor, Signaling pathways
in
Molecular and Cellular Neuroscience
volume
31
issue
4
pages
759 - 773
publisher
Elsevier
external identifiers
  • wos:000236659600015
  • scopus:33645356186
  • pmid:16503160
ISSN
1044-7431
DOI
10.1016/j.mcn.2006.01.001
language
English
LU publication?
yes
id
a0ed4b6d-4551-4c11-806e-66abb35d6e92 (old id 154974)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16503160&dopt=Abstract
date added to LUP
2016-04-04 08:56:30
date last changed
2021-09-08 02:15:19
@article{a0ed4b6d-4551-4c11-806e-66abb35d6e92,
  abstract     = {The rd1 mouse serves as a model for inherited photoreceptor degeneration: retinitis pigmentosa. Microarray techniques were employed to compare the transcriptomes of rd1 and congenic wild-type retinas at postnatal day 11, when degenerative processes have started but most photoreceptors are still present. Of the several genes that were differentially expressed, focus was put on those associated with the protein kinase C (PKC) signaling pathway, in particular PKCδ, μ and θ. Microarray identified these as being up-regulated in the rd1 retina, which was confirmed by QRT-PCR. Western blotting and immunostaining, using antibodies against either total or phosphorylated variants of the PKC isoforms, revealed increased expression and phosphorylation of PKCδ, μ and θ in the rd1 retina at the protein level as well. Our results suggest that these PKC isoforms are involved in rd1 degeneration.},
  author       = {Azadi, Seifollah and Paquet-Durand, Francois and Medstrand, Patrik and van Veen, Theo and Ekström, Per},
  issn         = {1044-7431},
  language     = {eng},
  number       = {4},
  pages        = {759--773},
  publisher    = {Elsevier},
  series       = {Molecular and Cellular Neuroscience},
  title        = {Up-regulation and increased phosphorylation of protein kinase C (PKC) delta, mu and theta in the degenerating rd1 mouse retina.},
  url          = {http://dx.doi.org/10.1016/j.mcn.2006.01.001},
  doi          = {10.1016/j.mcn.2006.01.001},
  volume       = {31},
  year         = {2006},
}