The Classical Complement Pathway Mediates Microglia-Dependent Remodeling of Spinal Motor Circuits during Development and in SMA is a research paper published in Cell Reports (2019). On theSindex it has a DataRank of 3.1. It has been cited 129 times, with 114 citing works in its 1-hop citation network.
Scored on demand from live citation data
Linked data & code
DataRank reads this dataset's downstream impact straight off the citation graph — no black box, no proprietary weighting. How is this computed?
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Base Score Contribution
0.730
From this paper's citation signal
Citation Network Contribution
2.4
From 100 citing papers with measurable signal
Ranked by each citer's contribution to N(p) — log1p(Cq) divided by its reference count — out of 114 citers.
National Institutes of Health
Grant: R01-NS078375
U.S. Department of Defense
Grant: GR.10235006
National Institute on Alcohol Abuse and Alcoholism
Grant: R01-AA027079
National Institutes of Health
Grant: 1R01AA027079-01
Mechanisms of synaptic loss by the classical complement pathway in motor circuit development and disease
National Institutes of Health
Grant: 1R01NS078375-01
Mechanisms of Central Synaptic Dysfunction in SMA
NIAAA NIH HHS
Grant: R01 AA027079
NINDS NIH HHS
Grant: R01 NS078375
FWCI
8.28
Citation Percentile
1.0%
Citation Trend
Fields of Study
MeSH Terms
Keywords
Additional file 1 of Increased chitotriosidase 1 concentration following nusinersen treatment in spinal muscular atrophy
Additional file 1 of Increased chitotriosidase 1 concentration following nusinersen treatment in spinal muscular atrophy
Additional file 2 of Increased chitotriosidase 1 concentration following nusinersen treatment in spinal muscular atrophy
Additional file 2 of Increased chitotriosidase 1 concentration following nusinersen treatment in spinal muscular atrophy
Additional file 3 of Increased chitotriosidase 1 concentration following nusinersen treatment in spinal muscular atrophy
Additional file 3 of Increased chitotriosidase 1 concentration following nusinersen treatment in spinal muscular atrophy