ArticleThe EMBO journal1996
Trans-acting factors regulate the expression of CD44 splice variants.
Article in The EMBO journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed, 53 citations in OpenAlex.
- Article
- Differential recruitment of CD44 isoforms by ErbB ligands reveals an involvement of CD44 in breast cancer.Oncogene · 2018Article
- CD44 mediates the catch-bond activated rolling of HEPG2Iso epithelial cancer cells on hyaluronan.Cell adhesion & migration · 2017Article
- Transforming growth factor β1 (TGFβ1) regulates CD44V6 expression and activity through extracellular signal-regulated kinase (ERK)-induced EGR1 in pulmonary fibrogenic fibroblasts.The Journal of biological chemistry · 2017Article
- CD82 suppresses CD44 alternative splicing-dependent melanoma metastasis by mediating U2AF2 ubiquitination and degradation.Oncogene · 2016Article
- CD44 functions in Wnt signaling by regulating LRP6 localization and activation.Cell death and differentiation · 2015Article
- Prognostic significance of CD44 variant 2 upregulation in colorectal cancer.British journal of cancer · 2014Article
- CD44v/CD44s expression patterns are associated with the survival of pancreatic carcinoma patients.Diagnostic pathology · 2014Article
- SC35 promotes splicing of the C5-V6-C6 isoform of CD44 pre-mRNA.Oncology reports · 2014Article
- Met receptors induce Sam68-dependent cell migration by activation of alternate extracellular signal-regulated kinase family members.The Journal of biological chemistry · 2011Article
- PCBP-1 regulates alternative splicing of the CD44 gene and inhibits invasion in human hepatoma cell line HepG2 cells.Molecular cancer · 2010Article
- Alternative splicing of G protein-coupled receptors: physiology and pathophysiology.Cellular and molecular life sciences : CMLS · 2009Review
- Regulation of CD44 alternative splicing by SRm160 and its potential role in tumor cell invasion.Molecular and cellular biology · 2006Article
- Analysis of the requirement for RNA polymerase II CTD heptapeptide repeats in pre-mRNA splicing and 3'-end cleavage.RNA (New York, N.Y.) · 2004Article
- CD44 in cancer progression: adhesion, migration and growth regulation.Journal of molecular histology · 2004Review
- CD44 is required for two consecutive steps in HGF/c-Met signaling.Genes & development · 2002Article
- Regulation of alternative pre-mRNA splicing by the ERK MAP-kinase pathway.The EMBO journal · 2001Article
- CD44 cell adhesion molecules.Molecular pathology : MP · 1999Review
- Growth and differentiation regulate CD44 expression on human keratinocytes.In vitro cellular & developmental biology. Animal · 1999Article
- Molecular studies into the role of CD44 variants in metastasis in gastric cancer.Molecular pathology : MP · 1999Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Variant isoforms of the cell surface glycoprotein CD44 (CD44v) are expressed during development, in selected adult tissues and in certain metastatic tumor cells. CD44v differ from the standard isoform (CD44s) by up to ten additional exon sequences included by alternative splicing. By cell fusion experiments, we have obtained evidence for the existence of cell-type specific trans-acting factors recruiting CD44 variant exon sequences. Stable cell hybrids of CD44s and CD44v expressing cells indicated a dominant mechanism for variant-exon inclusion. In transient interspecies heterokaryons of human keratinocytes and rat fibroblasts, the ability of the keratinocytes to include all variant exon sequences in CD44 was conferred completely on the rat fibroblast nucleus. Fusions of cells with complex CD44 splice patterns do not permit interpretation of splice control by the relative abundance of a single trans-acting factor, but rather by (a) positively acting factor(s) recruiting variant exon sequences in the 3' to 5' direction and additional factors selecting individual exons. Since the pancreatic carcinoma cell line BSp73ASML (in contrast to the cervix carcinoma cell lines SiHa and ME180) could not transfer its specific splice pattern in cell fusions, we conclude that in some tumors, splicing is also controlled by mutation of cis-acting recognition sites.
Indexed as
Identifiers
8670907PMC452123W19201180What 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.