Comparative proteomics in neurodegenerative and non-neurodegenerative diseases suggest nodal point proteins in regulatory networking.
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Comparative proteomics in neurodegenerative and non-neurodegenerative diseases suggest nodal point proteins in regulatory networking. / Zabel, Claus; Sagi, Dijana; Kaindl, Angela M; Steireif, Nicole; Kläre, Yvonne; Mao, Lei; Peters, Hartmut; Wacker, Maik A; Kleene, Ralf; Klose, Joachim.
in: J PROTEOME RES, Jahrgang 5, Nr. 8, 8, 2006, S. 1948-1958.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Comparative proteomics in neurodegenerative and non-neurodegenerative diseases suggest nodal point proteins in regulatory networking.
AU - Zabel, Claus
AU - Sagi, Dijana
AU - Kaindl, Angela M
AU - Steireif, Nicole
AU - Kläre, Yvonne
AU - Mao, Lei
AU - Peters, Hartmut
AU - Wacker, Maik A
AU - Kleene, Ralf
AU - Klose, Joachim
PY - 2006
Y1 - 2006
N2 - Neurodegenerative disorders (ND) encompass clinically and genetically heterogeneous diseases with considerable overlap of their clinical, neuropathological and molecular phenotype. Various causes of neurodegeneration in disease may affect eventually the same proteins within protein networks. To identify common changes in ND, we compared brain protein changes detected by 2-D electrophoresis in four mouse models for ND: (i) Parkinson's disease, (ii) Huntington's disease, (iii) prion disease Scrapie, and (iv) a model for impaired synaptic transmission. To determine specificity of these changes for ND, we extended the scope of our investigation to three neurological conditions that do not result in neurodegeneration (non-ND). We detected 12 to 216 consistent qualitative or quantitative protein changes in individual ND and non-ND models when compared to controls. Up to 36% of these proteins were found to be altered in multiple disease states (at least three) and were therefore termed nodal point proteins. Alterations in alpha B-Crystallin and splicing factor 3b (subunit 4) occurred in at least three ND but not in non-ND. In contrast, alterations in peroxiredoxin 1 and 3, astrocytic phosphoprotein PEA15, complexin 2 and aminoacylase 1 were common to both ND and non-ND. Finally, we investigated the expression pattern of the nodal point proteins in three inbred mouse strains and found different protein abundance (expression polymorphisms) in all cases. Nodal point proteins showing expression polymorphisms may be candidate proteins for disease associated modifiers.
AB - Neurodegenerative disorders (ND) encompass clinically and genetically heterogeneous diseases with considerable overlap of their clinical, neuropathological and molecular phenotype. Various causes of neurodegeneration in disease may affect eventually the same proteins within protein networks. To identify common changes in ND, we compared brain protein changes detected by 2-D electrophoresis in four mouse models for ND: (i) Parkinson's disease, (ii) Huntington's disease, (iii) prion disease Scrapie, and (iv) a model for impaired synaptic transmission. To determine specificity of these changes for ND, we extended the scope of our investigation to three neurological conditions that do not result in neurodegeneration (non-ND). We detected 12 to 216 consistent qualitative or quantitative protein changes in individual ND and non-ND models when compared to controls. Up to 36% of these proteins were found to be altered in multiple disease states (at least three) and were therefore termed nodal point proteins. Alterations in alpha B-Crystallin and splicing factor 3b (subunit 4) occurred in at least three ND but not in non-ND. In contrast, alterations in peroxiredoxin 1 and 3, astrocytic phosphoprotein PEA15, complexin 2 and aminoacylase 1 were common to both ND and non-ND. Finally, we investigated the expression pattern of the nodal point proteins in three inbred mouse strains and found different protein abundance (expression polymorphisms) in all cases. Nodal point proteins showing expression polymorphisms may be candidate proteins for disease associated modifiers.
KW - Animals
KW - Polymorphism, Genetic
KW - Mice
KW - Mice, Inbred C57BL
KW - Molecular Sequence Data
KW - Mice, Transgenic
KW - Mice, Inbred Strains
KW - Electrophoresis, Gel, Two-Dimensional
KW - Brain Chemistry
KW - Brain Diseases/genetics/metabolism
KW - Nerve Tissue Proteins/analysis/genetics
KW - Neurodegenerative Diseases/genetics/metabolism
KW - Proteomics
KW - Animals
KW - Polymorphism, Genetic
KW - Mice
KW - Mice, Inbred C57BL
KW - Molecular Sequence Data
KW - Mice, Transgenic
KW - Mice, Inbred Strains
KW - Electrophoresis, Gel, Two-Dimensional
KW - Brain Chemistry
KW - Brain Diseases/genetics/metabolism
KW - Nerve Tissue Proteins/analysis/genetics
KW - Neurodegenerative Diseases/genetics/metabolism
KW - Proteomics
M3 - SCORING: Journal article
VL - 5
SP - 1948
EP - 1958
JO - J PROTEOME RES
JF - J PROTEOME RES
SN - 1535-3893
IS - 8
M1 - 8
ER -
