Fibrillar α-synuclein induces neurotoxic astrocyte activation via RIP kinase signaling and NF-κB is a research paper published in Cell Death and Disease (2021). On theSindex it has a DataRank of 0.681. It has been cited 93 times.
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Base Score Contribution
0.681
From this paper's citation signal
Citation Network Contribution
0
Citation network not refreshed for this result
This paper's DataRank is currently driven only by its base citation score. Citation network data was not refreshed for this result.
Learn more about DataRank methodology →U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke
Grant: NS120895
National Institutes of Health
Grant: 3R01NS120895-01S1
Juan Angel_Diversity Supplement: R01 NS120895
NINDS NIH HHS
Grant: R01 NS120895
FWCI
8.35
Citation Percentile
1.0%
Citation Trend
Fields of Study
MeSH Terms
Keywords
Sustainable Development Goals
Additional file 1 of Prominent astrocytic alpha-synuclein pathology with unique post-translational modification signatures unveiled across Lewy body disorders
Additional file 1 of Prominent astrocytic alpha-synuclein pathology with unique post-translational modification signatures unveiled across Lewy body disorders
Additional file 2 of Prominent astrocytic alpha-synuclein pathology with unique post-translational modification signatures unveiled across Lewy body disorders
Additional file 2 of Prominent astrocytic alpha-synuclein pathology with unique post-translational modification signatures unveiled across Lewy body disorders
Additional file 6 of PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis
Additional file 6 of PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis
Additional file 1 of MLKL deficiency alleviates neuroinflammation and motor deficits in the α-synuclein transgenic mouse model of Parkinson’s disease
Additional file 1 of MLKL deficiency alleviates neuroinflammation and motor deficits in the α-synuclein transgenic mouse model of Parkinson’s disease
Additional file 1 of α-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce Cav3.2 calcium signaling in astrocytes
Additional file 1 of α-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce Cav3.2 calcium signaling in astrocytes
Additional file 2 of α-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce Cav3.2 calcium signaling in astrocytes
Additional file 2 of α-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce Cav3.2 calcium signaling in astrocytes
Additional file 3 of α-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce Cav3.2 calcium signaling in astrocytes
Additional file 3 of α-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce Cav3.2 calcium signaling in astrocytes
Additional file 4 of α-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce Cav3.2 calcium signaling in astrocytes
Additional file 4 of α-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce Cav3.2 calcium signaling in astrocytes
Additional file 8 of PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis
Additional file 8 of PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis
Additional file 4 of PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis
Additional file 5 of PI3K-AKT activation resculpts integrin signaling to drive filamentous tau-induced proinflammatory astrogliosis