ArticlePloS one2010
sel-11 and cdc-42, two negative modulators of LIN-12/Notch activity in C. elegans.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- RAP-2 and CNH-MAP4 Kinase MIG-15 confer resistance in bystander epithelium to cell-fate transformation by excess Ras or Notch activity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Redundant mechanisms regulating the proliferation vs. differentiation balance in theFrontiers in cell and developmental biology · 2022Review
- The role and therapeutic implication of endoplasmic reticulum stress in inflammatory cancer transformation.American journal of cancer research · 2022Review
- Reduction of Derlin activity suppresses Notch-dependent tumours in the C. elegans germ line.PLoS genetics · 2021Article
- Biology of theGenetics · 2019Review
- Quality Control in the Endoplasmic Reticulum: Crosstalk between ERAD and UPR pathways.Trends in biochemical sciences · 2018Review
- Functional Dysregulation of CDC42 Causes Diverse Developmental Phenotypes.American journal of human genetics · 2018Article
- Down-modulation of SEL1L, an unfolded protein response and endoplasmic reticulum-associated degradation protein, sensitizes glioma stem cells to the cytotoxic effect of valproic acid.The Journal of biological chemistry · 2014Article
- Spatial regulation of lag-2 transcription during vulval precursor cell fate patterning in Caenorhabditis elegans.Genetics · 2011Article
- mSEL-1L (Suppressor/enhancer Lin12-like) protein levels influence murine neural stem cell self-renewal and lineage commitment.The Journal of biological chemistry · 2011Article
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Authors and funding
3 authors.
Funding
Abstract
backgroundLIN-12/Notch signaling is important for cell-cell interactions during development, and mutations resulting in constitutive LIN-12/Notch signaling can cause cancer. Loss of negative regulators of lin-12/Notch activity has the potential for influencing cell fate decisions during development and the genesis or aggressiveness of cancer. METHODOLOGY/PRINCIPAL
findingsWe describe two negative modulators of lin-12 activity in C. elegans. One gene, sel-11, was initially defined as a suppressor of a lin-12 hypomorphic allele; the other gene, cdc-42, is a well-studied Rho GTPase. Here, we show that SEL-11 corresponds to yeast Hrd1p and mammalian Synoviolin. We also show that cdc-42 has the genetic properties consistent with negative regulation of lin-12 activity during vulval precursor cell fate specification. CONCLUSIONS/SIGNIFICANCE: Our results underscore the multiplicity of negative regulatory mechanisms that impact on lin-12/Notch activity and suggest novel mechanisms by which constitutive lin-12/Notch activity might be exacerbated in cancer.
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