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WormBase Tree Display for Gene: WBGene00000898

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Name Class

WBGene00000898SMapS_parentSequenceY55D5A
IdentityVersion1
NameCGC_namedaf-2Person_evidenceWBPerson521
Sequence_nameY55D5A.5
Molecular_name (19)
Other_nameCELE_Y55D5A.5Accession_evidenceNDBBX284603
Public_namedaf-2
DB_infoDatabase (14)
SpeciesCaenorhabditis elegans
HistoryVersion_change107 Apr 2004 11:29:21WBPerson1971EventImportedInitial conversion from geneace
StatusLive
Gene_info (12)
Disease_infoExperimental_modelDOID:9351Homo sapiensPaper_evidenceWBPaper00064218
Curator_confirmedWBPerson324
Date_last_updated07 Nov 2022 00:00:00
DOID:14330Homo sapiensPaper_evidenceWBPaper00045313
Curator_confirmedWBPerson324
Date_last_updated26 Jan 2015 00:00:00
Potential_model (37)
Disease_relevanceParkinson''s disease (PD) is an age-dependent neurodegenerative disease characterized by the accumulation of alpha-synuclein (alpha-syn) and the selective loss of dopamine (DA) neurons; studies in C. elegans models of alpha-syn proteotoxcity indicate that reduced IGF-1/insulin-like signaling (IIS) suppresses alpha-syn toxicity and DA neurodegeneration; specifically daf-2 mutant worms that overexpress human alpha-syn retain more wild-type DA neurons when compared to alpha-syn worms alone; mutants of daf-16/FOXO, a well-characterized downstream component of the IIS pathway enhanced neurodegeneration, and an intermediate level of neuroprotection was seen in daf-2; daf-16 double mutants overexpressing alpha-syn-GFP in DA neurons; further, RNA interference of glucose-6-phosphate isomerase (gpi-1/GPI), the glycolytic enzyme, enhanced alpha-syn-induced DA neurotoxicity, while it''s overexpression in DA neurons was neuroprotective; further studies in Drosophila and mice confirm that GPI is neuroprotective; these studies indicate that IIS signaling modulates alpha-syn induced DA neurodegeneration, across species.Homo sapiensPaper_evidenceWBPaper00045313
WBPaper00025083
WBPaper00031384
Curator_confirmedWBPerson324
Date_last_updated26 Jan 2015 00:00:00
In glucose-fed wild-type animals, the exponential like decline was restored in the active state, indicating that insulin signaling may be involved in regulation of fractal scaling of C. elegans behavior.Homo sapiensCurator_confirmedWBPerson324
Models_disease_in_annotationWBDOannot00000339
Models_disease_assertedWBDOannot00001356
Molecular_infoCorresponding_CDSY55D5A.5a
Y55D5A.5c
Y55D5A.5d
Y55D5A.5e
Y55D5A.5f
Y55D5A.5g
Corresponding_CDS_historyY55D5A.5:wp187
Y55D5A.5a:wp229
Y55D5A.5b:wp229
Y55D5A.5b:wp247
Corresponding_transcriptY55D5A.5b
Y55D5A.5a.1
Y55D5A.5c.1
Y55D5A.5d.1
Y55D5A.5e.1
Y55D5A.5f.1
Y55D5A.5g.1
Other_sequence (112)
Associated_feature (24)
Experimental_info (11)
Map_infoMapIIIPosition-8.03413Error0.111365
Well_ordered
PositiveInside_rearrnDf11
Positive_cloneC44B11
H05C05
Y55D5AInferred_automaticallyFrom sequence, transcript, pseudogene data
NegativeOutside_rearrtDf9
Mapping_data2_point273
411
412
7053
Multi_point (23)
Pos_neg_data (12)
Reference (1715)
PictureWBPicture0000013078
WBPicture0000013087
MethodGene