Table 2

Terms used in NeuroGeM
Terms Values Meaning
Organism D. melanogaster Three model organisms
C. elegans
S. cerevisiae
Gene ID FBgn------ Primary IDs used in the respective genome databases (FlyBase, WormBase, and SGD). These IDs are also used as primary IDs in NeuroGeM.
W--------
S---------
Type of modification Suppressor Suppressors are those genes that alleviate disease pathology or slow disease progression when over-expressed, and those that aggravate disease pathology or accelerate disease progression when down-regulated or deleted. Enhancers are those genes that alleviate disease pathology when down-regulated, and those that aggravate pathology when over-expressed. Non-modifiers have no effect on disease progression.
Enhancer
Non-modifier
Mode of action Toxicity modification Toxicity modifiers are those genes that change disease pathology. Aggregation modifiers are those genes that change the size or number of protein aggregates.
Aggregation modification
Disease model Alzheimer’s disease (AD) ND models compiled in the current version of NeuroGeM. We divided AD into the subtypes ADTau and AD according to the gene used to induce the disease phenotype (mutant Tau protein and Aβ42, respectively).
Huntington’s disease (HD)
Parkinson’s disease (PD)
Spinocerebellar ataxia type 1 (SCA1)
Spinocerebellar ataxia type 3 (SCA3)
Spinocerebellar ataxia type 7 (SCA7)
Amyotrophic lateral sclerosis (ALS)
PolyQ disease (PolyQ)
Disease induction Various This field contains expression cassette information described in the literature including promoter and disease-causing gene (e.g. polyQ stretch length).
Disease-causing mutant proteins compiled in NeuroGeM are Aβ and tau protein for AD, SOD1 for ALS, huntingtin for HD, α-synuclein for PD, Ataxin-1 for SCA1, Ataxin-3 (MJD) for SCA3, Ataxin-7 for SCA7 and polyQ stretches for the PolyQ disease model.
Modulation method Overexpression This field describes whether the expression level of the target gene increased (overexpression or gain-of-function) or decreased (knockdown, knockout, or loss-of-function). We adopted the same terms used in the original articles.
Gain-of-function
Knockdown
Knockout
Loss-of-function
Experimental scale Primary high-throughput This field describes the scale of the experiments. Experiments that were not high-throughput (HT) were assigned as low-throughput (LT). Experiments performed in primary screens were assigned as Primary high-throughput. Experiments to confirm the results obtained from the Primary high-throughput screens were assigned as Secondary high-throughput.
Secondary high-throughput
Low-throughput
Measurement Various This field describes how the change of pathology was evaluated. For example, change in the eye phenotype is a common readout in D. melanogaster, and cell growth rate is a common readout in S. cerevisiae.
Cell type Various This field briefly describes what cell lines and organs were utilized to carry out the experiment.

Na et al.

Na et al. BMC Medical Genomics 2013 6:52   doi:10.1186/1755-8794-6-52

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