HCSGD entry for CDKN2D


1. General information

Official gene symbolCDKN2D
Entrez ID1032
Gene full namecyclin-dependent kinase inhibitor 2D (p19, inhibits CDK4)
Other gene symbolsINK4D p19 p19-INK4D
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000079Regulation of cyclin-dependent protein serine/threonine kinase activityIDAbiological_process
GO:0000082G1/S transition of mitotic cell cycleIDAbiological_process
GO:0000278Mitotic cell cycleTASbiological_process
GO:0000731DNA synthesis involved in DNA repairIMPbiological_process
GO:0004861Cyclin-dependent protein serine/threonine kinase inhibitor activityIDAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIDAcellular_component
GO:0005737CytoplasmIDAcellular_component
GO:0005829CytosolTAScellular_component
GO:0006469Negative regulation of protein kinase activityIDAbiological_process
GO:0007050Cell cycle arrestIDAbiological_process
GO:0007605Sensory perception of soundIEAbiological_process
GO:0008285Negative regulation of cell proliferationIDAbiological_process
GO:0009411Response to UVIMPbiological_process
GO:0019901Protein kinase bindingIPImolecular_function
GO:0030308Negative regulation of cell growthIDAbiological_process
GO:0032526Response to retinoic acidIMPbiological_process
GO:0033280Response to vitamin DIMPbiological_process
GO:0042326Negative regulation of phosphorylationIDAbiological_process
GO:0043154Negative regulation of cysteine-type endopeptidase activity involved in apoptotic processIMPbiological_process
GO:0048102Autophagic cell deathIMPbiological_process
GO:0071901Negative regulation of protein serine/threonine kinase activityIDAbiological_process
GO:1902230Negative regulation of intrinsic apoptotic signaling pathway in response to DNA damageIMPbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.45617201470.47480600660.99999024731.0000000000

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

Data sourceUp or downLog fold change
GSE11954Down-0.2726165615
GSE13712_SHEARDown-0.1416245425
GSE13712_STATICUp0.1014785316
GSE19018Up0.1452834531
GSE19899_A1Down-0.0838944137
GSE19899_A2Down-0.0680163368
PubMed_21979375_A1Up0.3428326629
PubMed_21979375_A2Down-0.2902040603
GSE35957Down-0.3618263008
GSE36640Up0.0029220786
GSE54402Up0.0201607834
GSE9593Up0.1304810485
GSE43922Up0.0487738760
GSE24585Up0.5110421669
GSE37065Down-0.0594035138
GSE28863_A1Down-0.1950642708
GSE28863_A2Down-0.1416711211
GSE28863_A3Up0.1114908838
GSE28863_A4Up0.2303670353
GSE48662Up0.1616490601

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-215-5pMIMAT0000272MIRT024530MicroarrayFunctional MTI (Weak)19074876
hsa-miR-192-5pMIMAT0000222MIRT026171MicroarrayFunctional MTI (Weak)19074876
hsa-miR-26b-5pMIMAT0000083MIRT028887MicroarrayFunctional MTI (Weak)19088304
hsa-miR-331-3pMIMAT0000760MIRT043416CLASHFunctional 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

24667034The p19INK4d, a member of the family of cyclin-dependent kinase inhibitors (INK4), plays an important role on cell cycle regulation and in the cellular DNA damage response
24667034We hypothesize that p19INK4d is a potential factor involved in the onset and/or maintenance of the senescent state
24667034Changes in p19INK4d expression and localization during senescence were determined by Western blot and immunofluorescence assays
24667034RESULTS: The data presented here show for the first time that p19INK4d expression is up-regulated by different types of senescence
24667034Following a senescence stimulus, p19INK4d translocates to the nucleus and tightly associates with chromatin
24667034Moreover, reduced levels of p19INK4d impair senescence-related global genomic heterochromatinization
24667034Analysis of p19INK4d mRNA and protein levels in tissues from differently aged mice revealed an up-regulation of p19INK4d that correlates with age
24667034CONCLUSION: We propose that p19INK4d participates in the cellular mechanisms that trigger senescence by contributing to chromatin compaction
10851091Ubiquitin/proteasome-mediated degradation of p19INK4d determines its periodic expression during the cell cycle
10851091Assembly and activity of the proto-oncogenic cyclin D/CDK4(6) complexes, the major driving force of G1 phase progression, is negatively regulated by a family of INK4 CDK inhibitors p16INK4a, p15INK4b, p18INK4c, and p19INK4d
10851091Here we show that the periodic oscillation of the p19INK4d protein during the cell cycle is determined by the ubiquitin/proteasome-dependent mechanism, allowing the protein abundance to follow the changes in its mRNA expression
10851091Within the INK4 family, this regulatory mode appears restricted to p19INK4d whose ubiquitination was dependent on the integrity of lysine 62, and binding to CDK4
10851091These results highlight unexpected differences among the INK4 inhibitors, and suggest how p19INK4d may help regulate the rate of cyclin D/CDK4(6) complex formation, and thereby timely progression through the mammalian cell division cycle
9244355Both p18INK4c and p19INK4d were widely expressed during mouse embryogenesis, but p16INK4a and p15INK4b were not readily detected prenatally
9244355Although p15INK4b, p18INK4c and p19INK4d were demonstrated in many tissues by 4 weeks after birth, p16INK4a protein expression was restricted to the lung and spleen of older mice, with increased, more widespread mRNA expression during aging
9244355The levels of p16INK4a and p18INK4c, but not p15INK4b or p19INK4d, further increased as MEFs approached senescence
9244355Whereas p18INK4c and p19INK4d may regulate pre- and postnatal development, p16INK4a more likely plays a checkpoint function during cell senescence that underscores its selective role as a tumor suppressor
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