ArticleGenes & development2008
The kinesin KIF1Bbeta acts downstream from EglN3 to induce apoptosis and is a potential 1p36 tumor suppressor.
Article in Genes & development, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 159 papers, 3 of them syntheses that pooled it.
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.
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Who cites it
159 citing papers in PubMed, 3 syntheses or guidelines pooled it, 327 citations in OpenAlex.
- Association between KIF1B rs17401966 genetic polymorphism and hepatocellular carcinoma susceptibility: an updated meta-analysis.BMC medical genetics · 2019Pooled it
- Association between KIF1B rs17401966 polymorphism and hepatocellular carcinoma risk: a meta-analysis involving 17,210 subjects.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- Genetic polymorphism of the kinesin-like protein KIF1B gene and the risk of hepatocellular carcinoma.PloS one · 2013Pooled it
- Genetic and Clinical Profiles of Pheochromocytoma and Paraganglioma: A Single Center Study.Frontiers in endocrinology · 2020Trial
- Kinesins in Cancer Drug Resistance: Mechanisms, Therapeutic Targeting, and Translational Potential.Cancers · 2026Review
- Unveiling the Prevalence and Surgical Burden of Neurocristopathies: A Scoping Review and Statistical Analysis.Research square · 2026Article
- Article
- The evolving roles of pathologists in paragangliomas and pheochromocytomas.Virchows Archiv : an international journal of pathology · 2026Review
- Exploring Hepatocellular Carcinoma Pathogenesis: The Influence of Genetic Polymorphisms.Current pharmaceutical design · 2025Review
- Mechanisms and molecular characterization of relapsed/refractory neuroblastomas.Frontiers in oncology · 2025Review
- Research progress of kinesin family in neurological diseases.Frontiers in cellular neuroscience · 2025Review
- The Molecular Classification of Pheochromocytomas and Paragangliomas: Discovering the Genomic and Immune Landscape of Metastatic Disease.Endocrine pathology · 2024Review
- Genetic and Molecular Biomarkers in Aggressive Pheochromocytomas and Paragangliomas.International journal of molecular sciences · 2024Review
- CX‑5461 potentiates imatinib‑induced apoptosis in K562 cells by stimulatingExperimental and therapeutic medicine · 2024Article
- Case report: A rare DLST mutation in patient with metastatic pheochromocytoma: clinical implications and management challenges.Frontiers in oncology · 2024Article
- Management of pheochromocytomas and paragangliomas: Review of current diagnosis and treatment options.Cancer medicine · 2023Review
- Genetic predisposition and evolutionary traces of pediatric cancer risk: a prospective 5-year population-based genome sequencing study of children with CNS tumors.Neuro-oncology · 2023Article
- Genetic Susceptibility to Hepatocellular Carcinoma in Patients with Chronic Hepatitis Virus Infection.Viruses · 2023Review
- Comprehensive Pan-Cancer Analysis of KIF18A as a Marker for Prognosis and Immunity.Biomolecules · 2023Article
- Pheochromocytoma: a changing perspective and current concepts.Therapeutic advances in endocrinology and metabolism · 2023Review
99 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 10 institutions in 3 countries.
Funding
Abstract
VHL, NF-1, c-Ret, and Succinate Dehydrogenase Subunits B and D act on a developmental apoptotic pathway that is activated when nerve growth factor (NGF) becomes limiting for neuronal progenitor cells and requires the EglN3 prolyl hydroxylase as a downstream effector. Germline mutations of these genes cause familial pheochromocytoma and other neural crest-derived tumors. Using an unbiased shRNA screen we found that the kinesin KIF1Bbeta acts downstream from EglN3 and is both necessary and sufficient for neuronal apoptosis when NGF becomes limiting. KIF1Bbeta maps to chromosome 1p36.2, which is frequently deleted in neural crest-derived tumors including neuroblastomas. We identified inherited loss-of-function KIF1Bbeta missense mutations in neuroblastomas and pheochromocytomas and an acquired loss-of-function mutation in a medulloblastoma, arguing that KIF1Bbeta is a pathogenic target of these deletions.
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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.