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WormBase Tree Display for Gene: WBGene00000149

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Name Class

WBGene00000149SMapS_parentSequenceC42D8
IdentityVersion1
NameCGC_nameapl-1Person_evidenceWBPerson369
Sequence_nameC42D8.8
Molecular_nameC42D8.8a
C42D8.8a.1
CE04209
C42D8.8b
CE27845
C42D8.8b.1
Other_nameuvt-4
CELE_C42D8.8Accession_evidenceNDBBX284606
Public_nameapl-1
DB_infoDatabase (11)
SpeciesCaenorhabditis elegans
HistoryVersion_change107 Apr 2004 11:29:20WBPerson1971EventImportedInitial conversion from geneace
StatusLive
Gene_info (11)
Disease_infoExperimental_modelDOID:10652Homo sapiensPaper_evidenceWBPaper00037623
WBPaper00040923
WBPaper00041335
Accession_evidenceOMIM104300
Curator_confirmedWBPerson324
Date_last_updated21 Feb 2019 00:00:00
Potential_modelDOID:11832Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:620)
DOID:10652Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:620)
DOID:0081292Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:620)
DOID:0070028Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:620)
DOID:1561Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:620)
DOID:0080348Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:620)
DOID:9970Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:620)
DOID:824Homo sapiensInferred_automaticallyInferred by orthology to human genes with DO annotation (HGNC:620)
Disease_relevanceC. elegans is a model system to study the normal function of APP (Amyloid precursor protein) and it''s cleavage product beta-amyloid peptide, and their role in Alzheimer''s disease; elegans apl-1/APP, is essential for neuronal survival, either loss or overexpression of APL-1 causes lethality; neuronal overexpression of human beta-amyloid peptide in C. elegans, causes learning defects and muscle paralysis and intracellular accumulation of A-beta; further, reduced insulin/IGF-1 signaling protects against the pathogenic effects of A-beta.Homo sapiensPaper_evidenceWBPaper00040364
Curator_confirmedWBPerson324
Date_last_updated18 Jun 2013 00:00:00
Models_disease_in_annotationWBDOannot00000102
Models_disease_assertedWBDOannot00000630
WBDOannot00000631
Molecular_infoCorresponding_CDSC42D8.8a
C42D8.8b
Corresponding_transcriptC42D8.8a.1
C42D8.8b.1
Other_sequence (84)
Associated_feature (26)
Experimental_infoRNAi_result (29)
Expr_pattern (15)
Drives_construct (27)
Construct_product (29)
AntibodyWBAntibody00000473
WBAntibody00001222
WBAntibody00001223
Microarray_results (34)
Expression_cluster (232)
Interaction (104)
Map_infoMapXPosition-6.17972Error0.002702
PositivePositive_cloneC42D8Inferred_automaticallyFrom sequence, transcript, pseudogene data
NY#L14A
Mapping_dataMulti_point4158
Pseudo_map_position
Reference (84)
RemarkMap X
Following advice from JAH, uvt-4 was merged into apl-1 with apl-1 being kept as the primary name. These two genes were equivalent, though uvt is older. However, it was felt that more important recent work has been done using the name apl-1. Some of the information attached to the current apl-1 object therefore has been taken from the old uvt-4 Locus object.
Map 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