ArticleProceedings of the National Academy of Sciences of the United States of America1996
Activation of the human homologue of the Drosophila sina gene in apoptosis and tumor suppression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 100 citations in OpenAlex.
- Article
- Neural crest cells and fetal alcohol spectrum disorders: Mechanisms and potential targets for prevention.Pharmacological research · 2023Review
- mMolecular therapy. Nucleic acids · 2022Article
- Downregulation of Siah1 promotes colorectal cancer cell proliferation and migration by regulating AKT and YAP ubiquitylation and proteasome degradation.Cancer cell international · 2020Article
- MicroRNA-135a Protects Against Ethanol-Induced Apoptosis in Neural Crest Cells and Craniofacial Defects in Zebrafish by Modulating the Siah1/p38/p53 Pathway.Frontiers in cell and developmental biology · 2020Article
- STAT3 Potentiates SIAH-1 Mediated Proteasomal Degradation of β-Catenin in Human Embryonic Kidney Cells.Molecules and cells · 2016Article
- Investigating the molecular basis of Siah1 and Siah2 E3 ubiquitin ligase substrate specificity.PloS one · 2014Article
- α-Synuclein posttranslational modification and alternative splicing as a trigger for neurodegeneration.Molecular neurobiology · 2013Review
- Expression and clinical significance of SIAH in laryngeal squamous cell carcinoma.Medical oncology (Northwood, London, England) · 2013Article
- p53 Represses transcription of RING finger LIM domain-binding protein RLIM through Sp1.PloS one · 2013Article
- The role of tumor protein 53 mutations in common human cancers and targeting the murine double minute 2-p53 interaction for cancer therapy.Iranian journal of medical sciences · 2012Article
- Reciprocal repression between P53 and TCTP.Nature medicine · 2011Article
- Distinct expression patterns of the E3 ligase SIAH-1 and its partner Kid/KIF22 in normal tissues and in the breast tumoral processes.Journal of experimental & clinical cancer research : CR · 2010Article
- siah-1 Protein is necessary for high glucose-induced glyceraldehyde-3-phosphate dehydrogenase nuclear accumulation and cell death in Muller cells.The Journal of biological chemistry · 2010Article
- SIAH1 induced apoptosis by activation of the JNK pathway and inhibited invasion by inactivation of the ERK pathway in breast cancer cells.Cancer science · 2010Article
- Synphilin-1A inhibits seven in absentia homolog (SIAH) and modulates alpha-synuclein monoubiquitylation and inclusion formation.The Journal of biological chemistry · 2009Article
- The molecular programme of tumour reversion: the steps beyond malignant transformation.Nature reviews. Cancer · 2009Review
- Siah-1S, a novel splice variant of Siah-1 (seven in absentia homolog), counteracts Siah-1-mediated downregulation of beta-catenin.Oncogene · 2007Article
- Inactivating mutations of the Siah-1 gene in gastric cancer.Oncogene · 2004Article
- Translationally controlled tumor protein is a target of tumor reversion.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Developmentally regulated genes in Drosophila, which are conserved through evolution, are potential candidates for key functions in biological processes such as cell cycle, programmed cell death, and cancer. We report cloning and characterization of the human homologue of the Drosophila seven in absentia gene (HUMSIAH), which codes for a 282 amino acids putative zinc finger protein. HUMSIAH is localized on human chromosome 16q12-q13. This gene is activated during the physiological program of cell death in the intestinal epithelium. Moreover, human cancer-derived cells selected for suppression of their tumorigenic phenotype exhibit constitutively elevated levels of HUMSIAH mRNA. A similar pattern of expression is also displayed by the p21waf1. These results suggest that mammalian seven in absentia gene, which is a target for activation by p53, may play a role in apoptosis and tumor suppression.
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.