HCSGD entry for ERCC1


1. General information

Official gene symbolERCC1
Entrez ID2067
Gene full nameexcision repair cross-complementing rodent repair deficiency, complementation group 1 (includes overlapping antisense sequence)
Other gene symbolsCOFS4 RAD10 UV20
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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This gene isn't in Literature mining network.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000014Single-stranded DNA endodeoxyribonuclease activityIDAmolecular_function
GO:0000109Nucleotide-excision repair complexIDAcellular_component
GO:0000718Nucleotide-excision repair, DNA damage removalTASbiological_process
GO:0000720Pyrimidine dimer repair by nucleotide-excision repairIEAbiological_process
GO:0000737DNA catabolic process, endonucleolyticIDAbiological_process
GO:0000784Nuclear chromosome, telomeric regionIDAcellular_component
GO:0001094TFIID-class transcription factor bindingIEAmolecular_function
GO:0001302Replicative cell agingIEAbiological_process
GO:0003684Damaged DNA bindingIDA IEAmolecular_function
GO:0003697Single-stranded DNA bindingIDAmolecular_function
GO:0004519Endonuclease activityIEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIDA IEAcellular_component
GO:0005654NucleoplasmTAScellular_component
GO:0005669Transcription factor TFIID complexIEAcellular_component
GO:0005730NucleolusIDAcellular_component
GO:0005737CytoplasmIDAcellular_component
GO:0006281DNA repairIEA TASbiological_process
GO:0006283Transcription-coupled nucleotide-excision repairTASbiological_process
GO:0006289Nucleotide-excision repairIDA IGI TASbiological_process
GO:0006295Nucleotide-excision repair, DNA incision, 3'-to lesionIMPbiological_process
GO:0006296Nucleotide-excision repair, DNA incision, 5'-to lesionIMPbiological_process
GO:0006302Double-strand break repairIEAbiological_process
GO:0006310DNA recombinationIGIbiological_process
GO:0006312Mitotic recombinationIMPbiological_process
GO:0006949Syncytium formationIEAbiological_process
GO:0006979Response to oxidative stressIMPbiological_process
GO:0007281Germ cell developmentIEAbiological_process
GO:0007283SpermatogenesisIEAbiological_process
GO:0007584Response to nutrientIEAbiological_process
GO:0008022Protein C-terminus bindingIPImolecular_function
GO:0008283Cell proliferationIEAbiological_process
GO:0008584Male gonad developmentIEAbiological_process
GO:0009650UV protectionIEAbiological_process
GO:0009744Response to sucroseIEAbiological_process
GO:0010165Response to X-rayIEAbiological_process
GO:0010259Multicellular organismal agingIEAbiological_process
GO:0017025TBP-class protein bindingIEAmolecular_function
GO:0019904Protein domain specific bindingIPImolecular_function
GO:0032205Negative regulation of telomere maintenanceIMPbiological_process
GO:0035166Post-embryonic hemopoiesisIEAbiological_process
GO:0035264Multicellular organism growthIEAbiological_process
GO:0043566Structure-specific DNA bindingIDAmolecular_function
GO:0045190Isotype switchingIEAbiological_process
GO:0048477OogenesisIEAbiological_process
GO:0048568Embryonic organ developmentIEAbiological_process
GO:0051276Chromosome organizationIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.00665886930.88741463850.21426418091.0000000000

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Down-0.0497201013
GSE13712_SHEARDown-0.2079857879
GSE13712_STATICDown-0.0324592295
GSE19018Down-0.0374237969
GSE19899_A1Up1.6803362824
GSE19899_A2Up1.2534389262
PubMed_21979375_A1Up2.6782655852
PubMed_21979375_A2Up1.5389752848
GSE35957Down-0.1017654603
GSE36640Down-0.0588995938
GSE54402Up1.3851495762
GSE9593Up0.3097687345
GSE43922Up0.8077932219
GSE24585Up0.3512383038
GSE37065Down-0.0567732658
GSE28863_A1Down-0.0771028313
GSE28863_A2Down-0.1810375519
GSE28863_A3Down-0.4897509820
GSE28863_A4Up0.1101754295
GSE48662Down-0.0800290970

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-296-3pMIMAT0004679MIRT038492CLASHFunctional MTI (Weak)23622248
hsa-let-7b-5pMIMAT0000063MIRT052171CLASHFunctional MTI (Weak)23622248
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  • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 8 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

26464516To test our hypothesis, we combined experiments in mice with genomic instability resulting from the defective nucleotide excision repair gene ERCC1 (Ercc1(d/-) mice), human VSMC cultures and population genome-wide association studies (GWAS)
26102775DESIGN AND METHOD: Studies were performed in male and female Ercc1d/- mice and their wild type controls (Ercc1+/+) at the age of 12 or 18 weeks before and after treatment with losartan
26102775The ReninSense 680 probe showed increased intrarenal renin activity in Ercc1d/- mice versus Ercc1+/+ mice, both at 12 and 18 weeks of age, while PRC in these mice tended to be lower compared to Ercc1+/+ mice
26102775Renin was higher in male than female mice, both in the kidney and in plasma, and losartan increased kidney and plasma renin in both Ercc1d/- and Ercc1+/+ mice
25754370Periodic drug administration extended healthspan in Ercc1(-/) mice, delaying age-related symptoms and pathology, osteoporosis, and loss of intervertebral disk proteoglycans
24964749Involvement of ERCC1 in the pathogenesis of osteoarthritis through the modulation of apoptosis and cellular senescence
24964749In this study we investigated the function of ERCC1 in chondrocytes and its association with the pathophysiology of OA
24964749ERCC1 expression in normal and osteoarthritic cartilage was assessed, as were changes in ERCC1 expression in chondrocytes under catabolic stress
24964749Inhibiting ERCC1 in chondrocytes under interleukin-1beta stimulation using small interfering RNA (siRNA) was also evaluated
24964749Finally, cellular senescence and apoptosis were examined in relation to ERCC1 function
24964749ERCC1 expression was decreased in OA cartilage and increased within 4 h of exposure to interleukin (IL)-1beta, but decreased after 12 h
24964749The inhibition of ERCC1 by siRNA increased the expression of matrix metallopeptidase 13 and decreased collagen type II
24964749ERCC1 inhibition also increased the number of apoptotic and senescent cells
23852002XFE progeroid syndrome, a disease of accelerated aging caused by deficiency in the DNA repair endonuclease XPF-ERCC1, is modeled by Ercc1 knockout and hypomorphic mice
23852002We compared microRNA (miRNA) expression in Ercc1-/- primary mouse embryonic fibroblasts (MEFs) and wild-type (WT) MEFs in different growth conditions to identify miRNAs that drive cellular senescence
23852002Microarray analysis showed three differentially expressed miRNAs in passage 7 (P7) Ercc1-/- MEFs grown at 20% O2 compared to Ercc1-/- MEFs grown at 3% O2
23852002Thirty-six differentially expressed miRNAs were identified in Ercc1-/- MEFs at P7 compared to early passage (P3) in 3% O2
23281008Herein, we used progeroid ERCC1-XPF-deficient mice, including Ercc1-null (Ercc1(-/-)) and hypomorphic (Ercc1(-/Delta)) mice, to investigate the mechanism by which DNA damage leads to accelerated bone aging
23281008Compared to their wild-type littermates, both Ercc1(-/-) and Ercc1(-/Delta) mice display severe, progressive osteoporosis caused by reduced bone formation and enhanced osteoclastogenesis
23281008ERCC1 deficiency leads to atrophy of osteoblastic progenitors in the bone marrow stromal cell (BMSC) population
23281008Furthermore, we found that the transcription factor NF-kappaB is activated in osteoblastic and osteoclastic cells of the Ercc1 mutant mice
22705887METHODS AND RESULTS: In mice with genomic instability resulting from the defective nucleotide excision repair genes ERCC1 and XPD (Ercc1(d/-) and Xpd(TTD) mice), we explored age-dependent vascular function compared with that in wild-type mice
18083760Therefore, we summarize and discuss here that (i) systemic administration of anti-cancer chemotherapeutics, in many cases DNA cross-linking drugs, induces premature progeroid frailty in long-term survivors; (ii) that ICL-inducing 8-methoxy-psoralen/UVA phototherapy leads to signs of premature skin aging as prominent long-term side effect and (iii) that mutated factors involved in ICL repair like ERCC1/XPF, the Fanconi anaemia proteins, WRN and SNEV lead to reduced replicative life span in vitro and segmental progeroid syndromes in vivo
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