ArticleOncogene2016
Regulation of Numb isoform expression by activated ERK signaling.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 42 citations in OpenAlex.
- Tumoral switch in NUMB splicing changes essential transcription pathways and induces malignant properties in tumour cells.Genome biology · 2026Article
- Splicing regulatory dynamics for precision analysis and treatment of heterogeneous leukemias.Science translational medicine · 2025Article
- High expression of SRSF1 facilitates osteosarcoma progression and unveils its potential mechanisms.BMC cancer · 2024Article
- SPTAN1/NUMB axis senses cell density to restrain cell growth and oncogenesis through Hippo signaling.The Journal of clinical investigation · 2023Article
- PTBP1 promotes hepatocellular carcinoma progression by regulating the skipping of exon 9 in NUMB pre-mRNA.Heliyon · 2023Article
- Review
- Role of RNA Splicing in Regulation of Cancer Stem Cell.Current stem cell research & therapy · 2023Article
- Intronic Cis-Element DR8 in hTERT Is Bound by Splicing Factor SF3B4 and Regulates hTERT Splicing in Non-Small Cell Lung Cancer.Molecular cancer research : MCR · 2022Article
- Numb exon 9 inclusion regulates Integrinβ5 surface expression and promotes breast cancer metastasis.Oncogene · 2022Article
- Article
- Alternative RNA splicing in stem cells and cancer stem cells: Importance of transcript-based expression analysis.World journal of stem cells · 2021Review
- Modulation of alternative splicing during early infection of human primary B lymphocytes with Epstein-Barr virus (EBV): a novel function for the viral EBNA-LP protein.Nucleic acids research · 2021Article
- Asymmetric cell division of mammary stem cells.Cell division · 2021Review
- The role of NUMB/NUMB isoforms in cancer stem cells.BMB reports · 2021Review
- A splicing factor switch controls hematopoietic lineage specification of pluripotent stem cells.EMBO reports · 2021Article
- Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer.Bioscience reports · 2020Article
- An Intricate Connection between Alternative Splicing and Phenotypic Plasticity in Development and Cancer.Cells · 2019Review
- Exon 3 of theG3 (Bethesda, Md.) · 2019Article
- The ubiquitin ligase KBTBD8 regulates PKM1 levels via Erk1/2 and Aurora A to ensure oocyte quality.Aging · 2019Article
- NUMB and NUMBL differences in gene regulation.Oncotarget · 2018Article
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
Abstract
The endocytic adaptor protein Numb has a major role in development as an intrinsic regulator of cell fate determination and inhibitor of the Notch signaling pathway. In vertebrates, four protein isoforms of Numb are produced through alternative splicing (AS) of two cassette exons (exons 3 and 9). AS of coding exon 9 (E9) produces E9-included (p72/p71) and -excluded (p66/p65) protein products. Expression of Numb isoforms is developmentally regulated and E9-included products are expressed in progenitors, whereas E9-excluded isoforms are dominantly expressed in differentiated cells. Analyses of AS events in multiple cancers previously identified a switch in Numb transcript and protein expression from the E9-excluded to the E9-included isoform, suggesting that misregulation of the mechanisms that control E9 inclusion may have a role in tumorigenesis. Here we identify splicing factors ASF/SF2 and PTBP1 as regulators of E9 splicing and show that activation of the mitogen-activated protein kinase/extracellular signal-regulated kinase pathway promotes E9 inclusion in cancer cells. Our evidence supports a mechanism by which Numb AS is regulated in response to oncogenic signaling pathways, and contributes to activation of downstream pathways to promote tumorigenesis.
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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.