HCSGD entry for MRC1


1. General information

Official gene symbolMRC1
Entrez ID4360
Gene full namemannose receptor, C type 1
Other gene symbolsCD206 CLEC13D CLEC13DL MMR MRC1L1 bA541I19.1
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0004872Receptor activityIDAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005537Mannose bindingTASmolecular_function
GO:0005886Plasma membraneIDAcellular_component
GO:0005887Integral component of plasma membraneTAScellular_component
GO:0006898Receptor-mediated endocytosisIDAbiological_process
GO:0010008Endosome membraneIDAcellular_component
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.74570836590.21298672540.99999024730.8911180416

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

Data sourceUp or downLog fold change
GSE11954Down-0.0109772173
GSE13712_SHEARDown-0.2680251174
GSE13712_STATICDown-0.1080821670
GSE19018Down-0.0427665706
GSE19899_A1Up0.3192698177
GSE19899_A2Down-0.0121603635
PubMed_21979375_A1Up0.0637462545
PubMed_21979375_A2Up0.2009125627
GSE35957Down-0.4981393638
GSE36640Up0.2623713558
GSE54402Down-0.0329728058
GSE9593Down-0.8262456878
GSE43922Up0.0132665551
GSE24585Down-0.1282831632
GSE37065Down-0.0320077288
GSE28863_A1Down-0.1072571637
GSE28863_A2Down-0.1591885262
GSE28863_A3Up0.2691288945
GSE28863_A4Down-0.2453093839
GSE48662Up0.0825526562

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

    • mirTarBase
No target information from mirTarBase
    • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 6 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

18567801To determine the potential mechanisms of senescence-dependent increases in genomic instability, we analyzed DNA mismatch repair (MMR) efficiency in young and senescent human colonic fibroblast and human embryonic lung fibroblast
18567801It was found that MMR activity is significantly reduced in senescent cells
18567801Western blot and immunohistochemistry analysis revealed that hMSH2 and MSH6 protein (MutS alpha complex), which is a known key component in the MMR pathway, is markedly down-regulated in senescent cells
18567801Moreover, the addition of purified MutS alpha to extracts from senescent cells led to the restoration of MMR activity
18567801E2F1 small interfering RNA expression reduced hMSH2 expression and MMR activity in young human primary fibroblast cells
18567801Importantly, expression of E2F1 in quiescent cells restored the MSH2 expression as well as MMR activity, whereas E2F1-infected senescent cells exhibited no restoration of MSH2 expression and MMR activity
18567801These results indicate that the suppression of E2F1 transcriptional activity in senescent cells lead to stable repression of MSH2, followed by a induction of MutS alpha dysfunction, which results in a reduced cellular MMR capacity in senescent cells
18089797Furthermore, v5 was preferentially expressed in mismatch repair (MMR)-deficient cells and tumor tissues, suggesting its role in chromosome stability associated with MMR deficiency
16216462This study employed an in vitro model of human CD4+T cell ageing to investigate MMR capacity at various stages of T cell lifespan
16216462However, when challenged with supra-physiological levels of DNA mismatches, deficiencies were found in ageing T cell clones in MMR capacity, with the exception of T cell clones from a SENIEUR donor previously shown to maintain effective DNA excision repair
15760303Activation of Mrc1, a mediator of the replication checkpoint, by telomere erosion
15760303In telomerase-negative cells deleted for RAD9, Mrc1, another checkpoint adaptor previously implicated in the DNA replication checkpoint, mediated Rad53 activation
15760303However, unexpectedly, given the formation of an active Rad53-Mrc1 complex in tlc1Delta rad9Delta cells, Mrc1 did not mediate the cell-cycle arrest elicited by telomerase loss
15760303Finally, we report that Rad9, Mrc1, Dun1 and Chk1 are activated by phosphorylation after telomerase inactivation
15050284We showed significantly higher rates of microsatellite instability (MSI), an indicator of MMR dysfunction in older subjects, compared to young
11479224Temozolomide (TMZ) produces O(6)-methylguanine in DNA, which in turn mispairs with thymine, triggering futile DNA mismatch repair (MMR) and ultimately cell death
11479224We found previously that in p53-proficient human glioma cells, TMZ-induced futile DNA MMR resulted not in apoptosis but rather in prolonged, p53- and p21-associated G(2)-M arrest and senescence
11479224Taken together, these results indicate that Chk1 links TMZ-induced MMR to G(2)-M arrest
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