HCSGD entry for KIR2DL4

1. General information

Official gene symbolKIR2DL4
Entrez ID3805
Gene full namekiller cell immunoglobulin-like receptor, two domains, long cytoplasmic tail, 4
Other gene symbolsCD158D G9P KIR103 KIR103AS
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:0004888Transmembrane signaling receptor activityTASmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005886Plasma membraneTAScellular_component
GO:0005887Integral component of plasma membraneTAScellular_component
GO:0006968Cellular defense responseTASbiological_process
GO:0007165Signal transductionTASbiological_process
GO:0050776Regulation of immune responseTASbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.33697693860.92140170210.99999024731.0000000000

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

Data sourceUp or downLog fold change
GSE11954Up0.0659435348
GSE13712_SHEARUp0.1733246322
GSE13712_STATICDown-0.0163630384
GSE19018Up0.1089685842
GSE19899_A1Up0.0649128834
GSE19899_A2Up0.1317400798
PubMed_21979375_A1Up0.1625592622
PubMed_21979375_A2Up0.0408551905
GSE35957Up0.0737896351
GSE36640Up0.0569379927
GSE54402Down-0.0211449009
GSE9593Up0.1061264755
GSE43922--
GSE24585--
GSE37065--
GSE28863_A1Up0.3886348367
GSE28863_A2Down-0.0485615884
GSE28863_A3Up0.4108472379
GSE28863_A4Down-0.1071483168
GSE48662Down-0.1805159790

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: 3 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

26878797Here we show that ligands of an activating Natural Killer (NK) cell receptor (NKG2D), MICA and ULBP2 are consistently up-regulated following induction of replicative senescence, oncogene-induced senescence and DNA damage - induced senescence
24337384TNFR-associated factor 6 and TGF-beta-activated kinase 1 control signals for a senescence response by an endosomal NK cell receptor
24337384To understand how CD158d initiates signaling for a senescence response, we mapped the region in its cytoplasmic tail that controls signaling
24337384We identified a conserved TNFR-associated factor 6 (TRAF6) binding motif, which was required for CD158d-induced NF-kappaB activation and IL-8 secretion, TRAF6 association with CD158d, and TRAF6 recruitment to CD158d(+) endosomes in transfected cells
23184984Soluble HLA-G induces a proinflammatory response in primary, resting NK cells on endocytosis into early endosomes where its receptor, CD158d, resides
23184984CD158d initiates signaling through DNA-PKcs, Akt, and NF-kappaB for a proinflammatory and proangiogenic response
23184984The physiological relevance of this endosomal signaling pathway, and how activation of CD158d through soluble ligands regulates NK cell fate and function is unknown
23184984We show here that CD158d agonists trigger a DNA damage response signaling pathway involving cyclin-dependent kinase inhibitor p21 expression and heterochromatin protein HP1-gamma phosphorylation
23184984Sustained activation through CD158d induced morphological changes in NK cell shape and size, and survival in the absence of cell-cycle entry, all hallmarks of senescence, and a transcriptional signature of a senescence-associated secretory phenotype (SASP)
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