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Unread 04-16-2012, 06:59 PM   #1
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Default Pathways

Pathways - is anyone interested in running this thread with any pathways that are involved or suspected to be involved with pd?

from pipeline email

1. Neuronal RING finger protein 11 (RNF11) regulates canonical NF-kappaB signaling


The RING domain-containing protein RING finger protein 11 (RNF11) is a member of the A20 ubiquitin-editing protein complex and modulates peripheral NF-kappaB signaling. RNF11 is robustly expressed in neurons and colocalizes with a population of alpha-synuclein-positive Lewy bodies and neurites in Parkinson disease patients........

...........Conclusions: Our findings support the hypothesis that, in the nervous system, RNF11 negatively regulates canonical NF-kappaB signaling. Reduced or functionally compromised RNF11 could influence NF-kappaB-associated neuronal functions, including exaggerated inflammatory responses that may have implications for neurodegenerative disease pathogenesis and progression

more from:
over my head translators welcome

"Time is not neutral for those who have pd or for those who will get it."

Last edited by paula_w; 04-16-2012 at 07:40 PM.
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Unread 04-16-2012, 08:35 PM   #2
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Default Parkin, PINK and mt integrity: concept of mitochondrial dysfunction in PD

copied from madelyn


Leucine-rich repeat kinase 2 and alpha-synuclein: intersecting pathways in the pathogenesis of Parkinson's disease?
Elisa Greggio, Marco Bisaglia, Laura Civiero and Luigi Bubacco*

The electronic version of this article is the complete one and can be found online at: http://www.molecularneurodegeneration.com/content/6/1/6

Although Parkinson's disease (PD) is generally a sporadic neurological disorder, the discovery of monogenic, hereditable forms of the disease has been crucial in delineating the molecular pathways that lead to this pathology. Genes responsible for familial PD can be ascribed to two categories based both on their mode of inheritance and their suggested biological function. Mutations in parkin, PINK1 and DJ-1 cause of recessive Parkinsonism, with a variable pathology often lacking the characteristic Lewy bodies (LBs) in the surviving neurons. Intriguingly, recent findings highlight a converging role of all these genes in mitochondria function, suggesting a common molecular pathway for recessive Parkinsonism. Mutations in a second group of genes, encoding alpha-synuclein (α-syn) and LRRK2, are transmitted in a dominant fashion and generally lead to LB pathology, with α-syn being the major component of these proteinaceous aggregates. In experimental systems, overexpression of mutant proteins is toxic, as predicted for dominant mutations, but the normal function of both proteins is still elusive. The fact that α-syn is heavily phosphorylated in LBs and that LRRK2 is a protein kinase, suggests that a link, not necessarily direct, exists between the two. What are the experimental data supporting a common molecular pathway for dominant PD genes? Do α-syn and LRRK2 target common molecules? Does LRRK2 act upstream of α-syn? In this review we will try to address these of questions based on the recent findings available in the literature.

"Time is not neutral for those who have pd or for those who will get it."
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