GGrantIndex
← Leaderboards

Eric A Hendrickson

University Of Virginia

$12,783,397
Attributed
$13,005,459
Total exposure
10
Grants
9
Lead (contact PI)

Attributed= this PI's even-split share of every grant they're on (the fair, additive number). Exposure = full size of all those grants.

Funding over time

peak $1M · FY200525
$2M$1.5M$1M$500K$0
'05
'06
'07
'08
'09
'10
'11
'12
'13
'14
'15
'16
'17
'18
'19
'20
'21
'22
'23
'24
'25

Funding mix

By agency

NIH$13,005,459 · 10

By mechanism

R01$11,324,291 · 7
R21$851,633 · 2
P30$829,535 · 1

Top collaborators

Most similar at University Of Virginia

Same institution · by research overlap

Others in their field

Top investigators on “Genes

Research focus

GenesCell LineCellsMediatingSomatic CellGene TargetingPathway InteractionsDna RepairDouble Strand Break RepairDna Double Strand BreakNonhomologous Dna End JoiningHuman Cell LineApplications GrantsGenetic RecombinationTelomereGeneticLaboratoriesMissionResearch StudyMolecularMalignant NeoplasmsGenomeLoss Of Function MutationEvent

Grant awards (48)

POLQ- and CtIP-regulated telomere fusions and translocations are involved in early events in carcinogenesis$1,012,504
R01 · FY2025 · CA · contact PI
POLQ- and CtIP-regulated telomere fusions and translocations are involved in early events in carcinogenesis$480,791
R01 · FY2024 · CA · contact PI
Mechanism of radial chromosome formation in human premature aging syndrome cells$201,875
R21 · FY2024 · AG · contact PI
POLQ- and CtIP-regulated telomere fusions and translocations are involved in early events in carcinogenesis$499,539
R01 · FY2023 · CA · contact PI
Mechanism of radial chromosome formation in human premature aging syndrome cells$242,249
R21 · FY2023 · AG · contact PI
Genome Engineering Shared Resource$165,907
P30 · FY2023 · CA · contact PI
Mechanism of radial chromosome formation in human premature aging syndrome cells$1
R21 · FY2023 · AG · contact PI
POLQ- and CtIP-regulated telomere fusions and translocations are involved in early events in carcinogenesis$294,462
R01 · FY2022 · CA · contact PI
POLQ- and CtIP-regulated telomere fusions and translocations are involved in early events in carcinogenesis$216,859
R01 · FY2022 · CA · contact PI
Genome Engineering Shared Resource$165,907
P30 · FY2022 · CA · contact PI
Genome Engineering Shared Resource$165,907
P30 · FY2021 · CA · contact PI
Genome Engineering Shared Resource$165,907
P30 · FY2020 · CA · contact PI
Ligase III regulates survival from crisis induced by gradual telomere shortening$325,105
R01 · FY2019 · CA · contact PI
Genome Engineering Shared Resource$165,907
P30 · FY2019 · CA · contact PI
Ligase III regulates survival from crisis induced by gradual telomere shortening$335,160
R01 · FY2018 · CA · contact PI
The mechanism of Cas9/CRISPR-initiated genome modification in human somatic cells$283,657
R01 · FY2018 · GM · contact PI
Ligase III regulates survival from crisis induced by gradual telomere shortening$335,160
R01 · FY2017 · CA · contact PI
The mechanism of Cas9/CRISPR-initiated genome modification in human somatic cells$283,657
R01 · FY2017 · GM · contact PI
Ligase III regulates survival from crisis induced by gradual telomere shortening$335,160
R01 · FY2016 · CA · contact PI
The mechanism of Cas9/CRISPR-initiated genome modification in human somatic cells$283,657
R01 · FY2016 · GM · contact PI
Ligase III regulates survival from crisis induced by gradual telomere shortening$357,290
R01 · FY2015 · CA · contact PI
Ku regulates non-homologous end joining pathways in human somatic cells$310,678
R01 · FY2015 · CA · contact PI
The mechanism of Cas9/CRISPR-initiated genome modification in human somatic cells$283,657
R01 · FY2015 · GM · contact PI
Ku regulates non-homologous end joining pathways in human somatic cells$297,710
R01 · FY2014 · CA · contact PI
Ku regulates non-homologous end joining pathways in human somatic cells$18,872
R01 · FY2014 · CA · contact PI
Ku regulates non-homologous end joining pathways in human somatic cells$288,679
R01 · FY2013 · CA · contact PI
DNA Double-Strand Break Repair Regulates rAAV-Mediated Gene Targeting$273,758
R01 · FY2013 · GM · contact PI
Ku regulates non-homologous end joining pathways in human somatic cells$18,289
R01 · FY2013 · CA · contact PI
Ku regulates non-homologous end joining pathways in human somatic cells$307,286
R01 · FY2012 · CA · contact PI
DNA Double-Strand Break Repair Regulates rAAV-Mediated Gene Targeting$283,687
R01 · FY2012 · GM · contact PI
Ku regulates non-homologous end joining pathways in human somatic cells$15,504
R01 · FY2012 · CA · contact PI
Ku regulates non-homologous end joining pathways in human somatic cells$299,843
R01 · FY2011 · CA · contact PI
DNA Double-Strand Break Repair Regulates rAAV-Mediated Gene Targeting$283,687
R01 · FY2011 · GM · contact PI
Novel Human Cell Lines for the Study of Primary Immunodeficiencies$183,950
R21 · FY2011 · AI · contact PI
DNA Double-Strand Break Repair Regulates rAAV-Mediated Gene Targeting$286,553
R01 · FY2010 · GM · contact PI
Novel Human Cell Lines for the Study of Primary Immunodeficiencies$223,558
R21 · FY2010 · AI · contact PI
A human somatic cell model for Dyskeratosis Congenita$338,872
R01 · FY2008 · HL · contact PI
Ku86 Controls DNA Repair, Telomeres & Genomic Stability$239,023
R01 · FY2008 · GM · contact PI
A human somatic cell model for Dyskeratosis Congenita$339,254
R01 · FY2007 · HL · contact PI
Ku86 Controls DNA Repair, Telomeres & Genomic Stability$239,287
R01 · FY2007 · GM · contact PI
A human somatic cell model for Dyskeratosis Congenita$354,506
R01 · FY2006 · HL · contact PI
Ku86 Controls DNA Repair, Telomeres & Genomic Stability$246,698
R01 · FY2006 · GM · contact PI
A human somatic cell model for Dyskeratosis Congenita$358,567
R01 · FY2005 · HL
Ku86 Controls DNA Repair, Telomeres &Genomic Stability$250,816
R01 · FY2005 · GM
A human somatic cell model for Dyskeratosis Congenita$356,027
R01 · FY2004 · HL
KARP 1 V(D)J RECOMBINATION AND DNA REPAIR$174,042
R01 · FY2001 · AI
KARP 1 V(D)J RECOMBINATION AND DNA REPAIR$119,310
R01 · FY2001 · AI
KARP 1 V(D)J RECOMBINATION AND DNA REPAIR$296,685
R01 · FY2000 · AI