age-1;shc-1

Lifespan changes: From wild type to age-1;shc-1

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Genetic mutants with age-1, shc-1 alterations

    Names of genes are ordered alphabetically. For the order of interventions, please see the specific paper.
  • Temperature °C

    23

  • Diet

    NGM

  • Lifespan (days)

    17.5

  • Lifespan change (compared to wild type)

    23.24%

  • Phenotype

    age-1(hx546) completely suppressed the shortened life span of shc-1(ok198) as the double mutants had a mean life span similar to that of the long-lived age-1 mutants. This indicates that age-1 is epistatic to shc-1 and positions age-1 downstream from shc-1.

  • Lifespan comparisons

    Double mutant age-1(hx546);shc-1(ok198) has a lifespan of 17.5 days, while single mutant age-1(hx546) has a lifespan of 17.6 days, single mutant shc-1(ok198) has a lifespan of 8.4 days and wild type has a lifespan of 14.2 days.

  • Type of interaction
    See methods

    Contains dependence

  • Citation
    View abstract

    Neumann-Haefelin E et al., 2008, SHC-1/p52Shc targets the insulin/IGF-1 and JNK signaling pathways to modulate life span and stress response in C. elegans. Genes Dev. 22(19):2721-35 PubMed 18832074 Click here to select all mutants from this PubMed ID in the graph

Search genes: age-1 shc-1
  • Entrez ID
  • Symbol
  • GenAge
  • Wormbase ID

Phosphatidylinositol 3-kinase age-1;hypothetical protein


Locus: CELE_B0334.8


Wormbase description: age-1 encodes the C. elegans ortholog of the phosphoinositide 3-kinase (PI3K) p110 catalytic subunit; AGE-1, supplied maternally and embryonically, is a central component of the C. elegans insulin-like signaling pathway, lying downstream of the DAF-2/insulin receptor and upstream of both the PDK-1 and AKT-1/AKT-2 kinases and the DAF-16 forkhead type transcription factor, whose negative regulation is the key output of the insulin signaling pathway; in accordance with its role in insulin signaling, AGE-1 activity is required for regulation of metabolism, life span, dauer formation, stress resistance, salt chemotaxis learning, fertility, and embryonic development; although the age-1 expression pattern has not yet been reported, ectopic expression studies indicate that pan-neuronal age-1 expression is sufficient to rescue life-span defects, while neuronal, intestinal, or muscle expression can partially rescue dauer formation, and neuronal or muscle expression can rescue metabolic defects.


  • Entrez ID
  • Symbol
  • GenAge
  • Wormbase ID

SHC-transforming protein homolog 1


Locus: CELE_F54A5.3


Wormbase description: shc-1 encodes four proteins by multiple splicing, three of which are rather small (52-81 residues); however, one isoform (F54A5.3A, 316 residues) is a ortholog of vertebrate Shc proteins (e.g., p52/p46SHC and p66SHC); like its orthologs, F54A5.3A has a PTB and an SH2 domain in N- to C-terminal order; shc-1 interacts with both the JNK and insulin signaling pathways to regulate stress response and adult life span; SHC-1::GFP is widely expressed during postembryonic development and localizes to both the cytoplasm and the nucleus.


Orthologs of age-1;shc-1 in SynergyAge
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Species Gene
Orthologs of age-1 in SynergyAge
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Species Gene
Drosophila melanogaster Pi3K92E
Orthologs of shc-1 in SynergyAge
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Species Gene
About

SynergyAge database hosts high-quality, manually curated information about the synergistic and antagonistic lifespan effects of genetic interventions in model organisms, also allowing users to explore the longevity relationships between genes in a visual way.

Read more about SynergyAge database

How to cite us

If you would like to cite this database please use:

Bunu, G., Toren, D., Ion, C. et al. SynergyAge, a curated database for synergistic and antagonistic interactions of longevity-associated genes. Sci Data 7, 366 (2020). https://doi.org/10.1038/s41597-020-00710-z

Contact
Robi Tacutu, Ph.D.
Head: Systems Biology of Aging Group, Bioinformatics & Structural Biochemistry Department
Institute of Biochemistry, Ground floor
Splaiul Independentei 296, Bucharest, Romania
Email:

Group webpage: www.aging-research.group