ReviewCurrent molecular medicine2008
Menin, histone h3 methyltransferases, and regulation of cell proliferation: current knowledge and perspective.
Review in Current molecular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 40 citations in OpenAlex.
- Impaired transforming growth factor-β (TGF-β) transcriptional activity and cell proliferation control of a menin in-frame deletion mutant associated with multiple endocrine neoplasia type 1 (MEN1).The Journal of biological chemistry · 2012Trial
- Menin facilitates the cell proliferation of bladder cancer via modulating the TFAP2C/β-catenin axis.Genes & diseases · 2025Article
- Histone Modification on Parathyroid Tumors: A Review of Epigenetics.International journal of molecular sciences · 2022Review
- Pancreatic Neuroendocrine Neoplasms in Multiple Endocrine Neoplasia Type 1.International journal of molecular sciences · 2021Review
- Genomic Alterations in Sporadic Pituitary Tumors.Current neurology and neuroscience reports · 2018Review
- Epigenetic regulation by the menin pathway.Endocrine-related cancer · 2017Review
- Molecular markers of paragangliomas/pheochromocytomas.Oncotarget · 2017Review
- BRD4 inhibitor IBET upregulates p27kip/cip protein stability in neuroendocrine tumor cells.Cancer biology & therapy · 2017Article
- Loss of MEN1 activates DNMT1 implicating DNA hypermethylation as a driver of MEN1 tumorigenesis.Oncotarget · 2016Article
- Article
- Downregulation of tumor suppressor menin by miR-421 promotes proliferation and migration of neuroblastoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- A mechanistic role for the chromatin modulator, NAP1L1, in pancreatic neuroendocrine neoplasm proliferation and metastases.Epigenetics & chromatin · 2014Article
- Menin-mediated regulation of miRNA biogenesis uncovers the IRS2 pathway as a target for regulating pancreatic beta cells.Oncoscience · 2014Article
- Identification of somatic mutations in parathyroid tumors using whole-exome sequencing.The Journal of clinical endocrinology and metabolism · 2012Article
- Menin and JunD regulate gastrin gene expression through proximal DNA elements.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Article
- Article
- Article
- Lung cancer cell migration is regulated via repressing growth factor PTN/RPTP β/ζ signaling by menin.Oncogene · 2010Article
- MLL2 is required in oocytes for bulk histone 3 lysine 4 trimethylation and transcriptional silencing.PLoS biology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Menin is a tumor suppressor encoded by the MEN1 gene that is mutated in patients with an inherited syndrome, multiple endocrine neoplasia type 1 (MEN1). Loss of menin has potent impact on proliferation of endocrine and non-endocrine cells. However, until recently little has been known as to how menin regulates cell proliferation. Rapid research progress in the past several years suggests that menin represses proliferation of endocrine cells yet promotes proliferation in certain types of leukemia cells via interacting with various transcriptional regulators. Menin interacts with histone H3 methyltransferases such as MLL (mixed lineage leukemia) protein. Increasing evidence has linked the biological function of menin to epigenetic histone modifications, control of the pattern of gene expression, and regulation of cell proliferation in a cell type-specific manner. In light of these recent findings, an emerging model suggests that menin is a crucial regulator of histone modifiers by acting as a scaffold protein to coordinate gene transcription and cell proliferation in a cell context-dependent manner. This recent progress unravels the coordinating role of menin in epigenetics and regulation of cell cycle, providing novel insights into understanding regulation of beta cell functions and diabetes, as well as the development and therapy of endocrine tumors and leukemia.
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.