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WormBase Tree Display for Gene: WBGene00000407

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Name Class

WBGene00000407EvidenceAccession_evidenceEMBLAF129111
SMapS_parentSequenceT27E9
IdentityVersion1
NameCGC_namecdk-5Person_evidenceWBPerson346
Sequence_nameT27E9.3
Molecular_nameT27E9.3
T27E9.3.1
CE21213
Other_nameCELE_T27E9.3Accession_evidenceNDBBX284603
Public_namecdk-5
DB_infoDatabase (14)
SpeciesCaenorhabditis elegans
HistoryVersion_change107 Apr 2004 11:29:20WBPerson1971EventImportedInitial conversion from geneace
StatusLive
Gene_infoBiotypeSO:0001217
Gene_classcdk
Reference_alleleWBVar00239195
Allele (41)
StrainWBStrain00031527
WBStrain00007494
RNASeq_FPKM (74)
GO_annotation (49)
Ortholog (35)
Paralog (18)
Structured_descriptionConcise_descriptioncdk-5 encodes a proline-directed protein serine/threonine kinase homologous to cyclin dependent kinase 5 (CDK5); in ventral cord interneurons, CDK-5 activity regulates the subcellular localization of LIN-10 which, in turn, regulates the synaptic localization of the GLR-1 glutamate receptor; cdk-5 also regulates the polarized distribution of neuropeptide-containing dense core vesicles in cholinergic motor neurons; CDK-5 phosphorylates LIN-10 in vitro.Paper_evidenceWBPaper00040649
WBPaper00030893
WBPaper00041192
Curator_confirmedWBPerson48
WBPerson1843
Date_last_updated04 Feb 2013 00:00:00
Automated_descriptionEnables protein kinase activity. Involved in several processes, including GABAergic synaptic transmission; regulation of cellular localization; and regulation of synapse organization. Located in axon and synapse. Used to study epilepsy and lissencephaly. Human ortholog(s) of this gene implicated in Alzheimer's disease and lissencephaly 7 with cerebellar hypoplasia. Is an ortholog of human CDK5 (cyclin dependent kinase 5).Paper_evidenceWBPaper00065943
Curator_confirmedWBPerson324
WBPerson37462
Inferred_automaticallyThis description was generated automatically by a script based on data from the WS291 version of WormBase
Date_last_updated29 Nov 2023 00:00:00
Disease_infoExperimental_modelDOID:1826Homo sapiensPaper_evidenceWBPaper00028525
Curator_confirmedWBPerson324
Date_last_updated24 Aug 2021 00:00:00
DOID:0050453Homo sapiensPaper_evidenceWBPaper00028525
Accession_evidenceOMIM607432
Curator_confirmedWBPerson324
Date_last_updated17 Apr 2013 00:00:00
Potential_modelDOID:10652Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:1774)
DOID:0112231Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:1774)
Disease_relevanceIn humans, mutations in the LIS1 gene (Platelet activating factor acetylhydrolase, isoform 1B, alpha subunit; PAFAH1B1) and the LIS1 pathway, are implicated in Lissencephaly, a developmental abnormality associated with a failure of neuronal migration in the cerebral cortex, leading to mental retardation and epilepsy; human NDE1 and NDEL1, are effectors of LIS1; the elegans genetic model for epileptic siezures consists of lis-1 mutants that are responsive to the common seizure inducer pentylenetetrazole (PTZ) and diplay a distinct convulsive phenotype; studies in the worm show that cdk-5 (orthologous to human CDK5), is a LIS1 pathway component and worms depleted for LIS1 pathway components via RNA interference: NUD-1, NUD-2, DHC-1, CDK-5, and CDKA-1, also exhibited significant convulsions following PTZ treatment; further nud-1 (orthologous to human NUDC), nud-2/NDE1 and cdk-5 show significant enhancement in convulsions in a lis-1 heterozygous background when compared with the wild-type background; these animals are also less likely to recover when PTZ treatment is removed, when compared to wild-type; these studies show that while knocking down target genes (lis-1, cdk-5, and cdka-1 that function in neuronal migration), and their interacting proteins like nud-1, nud-2 and dhc-1, does not yield spontaneous convulsions in C. elegans, further alterations in the neural environment through the application of PTZ serve to pass a critical threshold within these animals.Homo sapiensCurator_confirmedWBPerson324
Models_disease_in_annotationWBDOannot00000151
WBDOannot00001013
Molecular_infoCorresponding_CDST27E9.3
Corresponding_transcriptT27E9.3.1
Other_sequenceAF129111
Associated_featureWBsf651579
WBsf667584
WBsf667585
WBsf667586
WBsf667587
WBsf994897
WBsf994898
WBsf1016373
WBsf227752
WBsf227753
Experimental_infoRNAi_resultWBRNAi00086131Inferred_automaticallyRNAi_primary
WBRNAi00006102Inferred_automaticallyRNAi_primary
WBRNAi00111862Inferred_automaticallyRNAi_primary
WBRNAi00019344Inferred_automaticallyRNAi_primary
WBRNAi00061488Inferred_automaticallyRNAi_primary
WBRNAi00076721Inferred_automaticallyRNAi_primary
WBRNAi00054326Inferred_automaticallyRNAi_primary
WBRNAi00036039Inferred_automaticallyRNAi_primary
Expr_patternExpr9053
Expr1020175
Expr1030224
Expr1157873
Expr2009812
Expr2028053
Drives_constructWBCnstr00037564
Construct_product (15)
Microarray_results (22)
Expression_cluster (120)
Interaction (91)
Map_infoMapIIIPosition21.2193Error0.000237
PositivePositive_cloneT27E9Inferred_automaticallyFrom CDS info
From sequence, transcript, pseudogene data
Mapping_dataMulti_point4197
Pseudo_map_position
Reference (48)
RemarkMap position created from combination of previous interpolated map position (based on known location of sequence) and allele information. Therefore this is not a genetic map position based on recombination frequencies or genetic experiments. This was done on advice of the CGC.CGC_data_submission
MethodGene