ArticleThe Journal of biological chemistry2012
Characterization of CSL (CBF-1, Su(H), Lag-1) mutants reveals differences in signaling mediated by Notch1 and Notch2.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 46 citations in OpenAlex.
- Association between the TP63 and CIR1 polymorphisms and non-small cell lung cancer in Chinese population.Journal of cardiothoracic surgery · 2026Article
- Role of Notch signaling in corticalization.Journal of endocrinological investigation · 2026Review
- The cellular Notch1 protein promotes KSHV reactivation in an Rta-dependent manner.Journal of virology · 2024Article
- Unraveling paralog-specific Notch signaling through thermodynamics of ternary complex formation and transcriptional activation of chimeric receptors.Protein science : a publication of the Protein Society · 2024Article
- The structure, binding and function of a Notch transcription complex involving RBPJ and the epigenetic reader protein L3MBTL3.Nucleic acids research · 2022Article
- A Drosophila Su(H) model of Adams-Oliver Syndrome reveals cofactor titration as a mechanism underlying developmental defects.PLoS genetics · 2022Article
- Interaction between BEND5 and RBPJ suppresses breast cancer growth and metastasis via inhibiting Notch signaling.International journal of biological sciences · 2022Article
- A brief overview of clinical significance of novel Notch2 regulators.Molecular & cellular oncology · 2020Review
- The Skeleton of Lateral Meningocele Syndrome.Frontiers in genetics · 2020Review
- Structurally conserved binding motifs of transcriptional regulators to notch nuclear effector CSL.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- CSL controls telomere maintenance and genome stability in human dermal fibroblasts.Nature communications · 2019Article
- The evolution of transcriptional repressors in the Notch signaling pathway: a computational analysis.Hereditas · 2019Article
- Notch in skeletal physiology and disease.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2018Review
- The lateral meningocele syndrome mutation causes marked osteopenia in mice.The Journal of biological chemistry · 2018Article
- Article
- Induction of the Hajdu-Cheney Syndrome Mutation in CD19 B Cells in Mice Alters B-Cell Allocation but Not Skeletal Homeostasis.The American journal of pathology · 2018Article
- Clinical and experimental aspects of notch receptor signaling: Hajdu-Cheney syndrome and related disorders.Metabolism: clinical and experimental · 2018Review
- RBPJ/CBF1 interacts with L3MBTL3/MBT1 to promote repression of Notch signaling via histone demethylase KDM1A/LSD1.The EMBO journal · 2017Article
- Article
- Sustained Notch2 signaling in osteoblasts, but not in osteoclasts, is linked to osteopenia in a mouse model of Hajdu-Cheney syndrome.The Journal of biological chemistry · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Notch is a conserved signaling pathway that plays essential roles during embryonic development and postnatally in adult tissues; misregulated signaling results in human disease. Notch receptor-ligand interactions trigger cleavage of the Notch receptor and release of its intracellular domain (NICD) from the membrane. NICD localizes to the nucleus where it forms a transcriptionally active complex with the DNA-binding protein CSL and the coactivator Mastermind (MAM) to up-regulate transcription from Notch target genes. Previous studies have determined the structure of the CSL-NICD-MAM ternary complex and characterized mutations that affect complex assembly in functional assays. However, as CSL is expressed in all cell types, these studies have been limited to analyzing mutations in NICD and MAM. Here, we describe a novel set of cellular reagents to characterize how mutations in CSL affect its function as a transcriptional activator. Using retrovirally transduced embryonic fibroblasts from a CSL-null mouse, we generated cell lines that express either wild-type or mutant CSL molecules. We then analyzed these mutants for defects in Notch1- (NICD1) or Notch2 (NICD2)-mediated activation from two different transcriptional reporters (HES-1 or 4×CBS). Our results show that mutations targeted to the different domains of CSL display significant differences in their ability to adversely affect transcription from the two reporters. Additionally, a subset of CSL mutants is sensitive to whether NICD1 or NICD2 was used to activate the reporter. Taken together, these studies provide important molecular insights into how Notch transcription complexes assemble at different target genes and promoter arrangements in vivo.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.