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WormBase Tree Display for Gene: WBGene00003829

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Name Class

WBGene00003829SMapS_parentSequenceF53A2
IdentityVersion1
NameCGC_namenud-1Person_evidenceWBPerson87
Sequence_nameF53A2.4
Molecular_nameF53A2.4
F53A2.4.1
CE16096
Other_nameCELE_F53A2.4Accession_evidenceNDBBX284603
Public_namenud-1
DB_infoDatabase (11)
SpeciesCaenorhabditis elegans
HistoryVersion_change107 Apr 2004 11:29:33WBPerson1971EventImportedInitial conversion from geneace
StatusLive
Gene_infoBiotypeSO:0001217
Gene_classnud
Allele (18)
StrainWBStrain00035169
WBStrain00031486
RNASeq_FPKM (74)
GO_annotation (15)
Contained_in_operonCEOP3784
Ortholog (36)
Structured_descriptionConcise_descriptionnud-1 encodes the C. elegans ortholog of the Aspergillus nidulans nudC, which mediates nuclear migration along Aspergillus hyphae.Paper_evidenceWBPaper00004895
Curator_confirmedWBPerson567
Date_last_updated17 Jun 2004 00:00:00
Automated_descriptionEnables identical protein binding activity and unfolded protein binding activity. Involved in several processes, including GABAergic synaptic transmission; chaperone-mediated protein folding; and establishment of organelle localization. Predicted to be located in cytoplasm. Expressed in gonad; hypodermis; intestine; and neurons. Used to study epilepsy and lissencephaly. Is an ortholog of human NUDC (nuclear distribution C, dynein complex regulator).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
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; 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 sapiensPaper_evidenceWBPaper00024523
WBPaper00028525
Accession_evidenceOMIM601545
Curator_confirmedWBPerson324
Models_disease_in_annotationWBDOannot00000148
WBDOannot00001010
Molecular_infoCorresponding_CDSF53A2.4
Corresponding_transcriptF53A2.4.1
Other_sequence (82)
Associated_featureWBsf994858
WBsf994859
WBsf225989
Experimental_infoRNAi_result (22)
Expr_patternExpr2419
Expr10134
Expr1011738
Expr1031804
Expr1151858
Expr2014524
Expr2032763
Drives_constructWBCnstr00000117
Construct_productWBCnstr00007338
Microarray_results (20)
Expression_cluster (141)
Interaction (45)
Map_infoMapIIIPosition21.2108Error0.000119
PositivePositive_cloneF53A2Inferred_automaticallyFrom sequence, transcript, pseudogene data
Mapping_dataMulti_point4503
4549
Pseudo_map_position
Reference (23)
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