HCSGD entry for SPRY1


1. General information

Official gene symbolSPRY1
Entrez ID10252
Gene full namesprouty homolog 1, antagonist of FGF signaling (Drosophila)
Other gene symbolshSPRY1
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:0001656Metanephros developmentIEAbiological_process
GO:0001657Ureteric bud developmentIEAbiological_process
GO:0001759Organ inductionIEAbiological_process
GO:0005515Protein bindingIPImolecular_function
GO:0005829CytosolTAScellular_component
GO:0005886Plasma membraneTAScellular_component
GO:0007173Epidermal growth factor receptor signaling pathwayTASbiological_process
GO:0008285Negative regulation of cell proliferationIEAbiological_process
GO:0034261Negative regulation of Ras GTPase activityIEAbiological_process
GO:0040037Negative regulation of fibroblast growth factor receptor signaling pathwayIEAbiological_process
GO:0042059Negative regulation of epidermal growth factor receptor signaling pathwayTASbiological_process
GO:0043407Negative regulation of MAP kinase activityIEAbiological_process
GO:0046580Negative regulation of Ras protein signal transductionIEAbiological_process
GO:0051387Negative regulation of neurotrophin TRK receptor signaling pathwayIEAbiological_process
GO:0070373Negative regulation of ERK1 and ERK2 cascadeIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.12752669730.03257271380.72694851700.3404870532

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

Data sourceUp or downLog fold change
GSE11954Down-0.3364597076
GSE13712_SHEARDown-1.0554268715
GSE13712_STATICDown-1.2985005264
GSE19018Up0.3771379975
GSE19899_A1Down-0.4700216940
GSE19899_A2Down-0.4918521547
PubMed_21979375_A1Up0.4539634623
PubMed_21979375_A2Up1.1604697943
GSE35957Up0.0254523365
GSE36640Up0.3176506897
GSE54402Down-0.9690161717
GSE9593Up0.0280982516
GSE43922Up0.0923591524
GSE24585Down-0.6293203928
GSE37065Down-0.2528659659
GSE28863_A1Up0.7878852802
GSE28863_A2Up0.9526973519
GSE28863_A3Up0.0425554904
GSE28863_A4Down-0.0535939994
GSE48662Up0.3999886035

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-98-5pMIMAT0000096MIRT027552MicroarrayFunctional MTI (Weak)19088304
hsa-miR-26b-5pMIMAT0000083MIRT029134MicroarrayFunctional MTI (Weak)19088304
hsa-miR-324-3pMIMAT0000762MIRT042959CLASHFunctional MTI (Weak)23622248
hsa-miR-3615MIMAT0017994MIRT052850CLASHFunctional 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: 3 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

27000748DNA hypomethylation at the SPRY1 gene locus downregulates sprouty1, causing inability to maintain quiescence and eventual exhaustion of the stem cell population
26526994Age-Associated Methylation Suppresses SPRY1, Leading to a Failure of Re-quiescence and Loss of the Reserve Stem Cell Pool in Elderly Muscle
26526994We link aging to an increased methylation of the SPRY1 gene, a known regulator of muscle stem cell quiescence
26526994Replenishment of the reserve cell pool was modulated experimentally by demethylation or siRNA knockdown of SPRY1
26526994We propose that suppression of SPRY1 by age-associated methylation in humans inhibits the replenishment of the muscle stem cell pool, contributing to a decreased regenerative response in old age
24270409In the present work, we describe a novel mechanism by which Spry1 restricts proliferation, independently of the ERK pathway
24270409In vivo analysis of thyroid glands from Spry1 knockout mice reveals that Spry1 induces a senescence-associated secretory phenotype via activation of the NFkappaB pathway
24270409Consistently, thyroids from Spry1 knockout mice are bigger and exhibit decreased markers of senescence including Ki67 labeling and senescence-associated beta-galactosidase
24270409Although such 'escape' from senescence is not sufficient to promote thyroid tumorigenesis in adult mice up to 5 months, the onset of Phosphatase and tensin homolog (Pten)-induced tumor formation is accelerated when Spry1 is concomitantly eliminated
24270409Accordingly, we observe a reduction of SPRY1 levels in human thyroid malignancies when compared with non-tumoral tissue
24270409We propose that Spry1 acts as a sensor of mitogenic activity that not only attenuates RTK signaling but also induces a cellular senescence response to avoid uncontrolled proliferation
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