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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Meningioma

MN1, MNI, Incw2
Meningioma 1 (MN1) contains two sets of CAG repeats. It is disrupted by a balanced translocation (4;22) in a meningioma, and its inactivation may contribute to meningioma 32 pathogenesis. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, HAD, ACID, FLT3, BAALC
Papers using MN1 antibodies
Functional imaging with cellular resolution reveals precise micro-architecture in visual cortex.
Supplier
Degtyar Vadim E., In PLoS ONE, 2004
An aliquot of MNI-caged-L-glutamate (4-methoxy-7-nitroindolinyl-caged L-glutamate, Tocris Bioscience, Ellisville, MO) was ...
Rapid reversible changes in dendritic spine structure in vivo gated by the degree of ischemia
Supplier
Shepherd Gordon M. G. et al., In Frontiers in Neural Circuits, 2004
... Slices were bathed with ACSF containing MNI-glutamate (0.2 mM, Tocris), MgCl ...
Papers on MN1
Wenyingzhuangia aestuarii sp. nov., A Marine Bacterium of the Family Flavobacteriaceae Isolated from an Estuary.
New
Kasai et al., Taegu, South Korea. In Curr Microbiol, Jan 2016
UNASSIGNED: A Gram-negative, strictly aerobic, chemoheterotrophic, pale-yellow pigmented, non-motile, rod-shaped bacterial strain, designated MN1-138(T), was isolated from water in the tidal zone at the estuary of Heita river, Iwate, Japan, using an in situ cultivation technique.
Microdeletion del(22)(q12.1) excluding the MN1 gene in a patient with craniofacial anomalies.
New
Coutton et al., Grenoble, France. In Am J Med Genet A, Dec 2015
UNASSIGNED: Several studies have recently reported that 22q12.1 deletions encompassing the MN1 gene are associated with craniofacial anomalies.
Expression of a passenger miR-9* predicts favorable outcome in adults with acute myeloid leukemia less than 60 years of age.
New
Jongen-Lavrencic et al., Rotterdam, Netherlands. In Leukemia, Nov 2015
Comparative transcriptome analysis suggests that miR-9* regulates genes involved in leukemogenesis, for example, MN1 and MLLT3.
MN1-Fli1 oncofusion transforms murine hematopoietic progenitor cells into acute megakaryoblastic leukemia cells.
Mikesch et al., Münster, Germany. In Oncogenesis, 2014
Recently, an in-frame fusion of meningeoma 1-friend leukemia virus integration 1 (MN1-Fli1) gene was detected in a child with AMKL.
Sixteen new lung function signals identified through 1000 Genomes Project reference panel imputation.
Tobin et al., London, United Kingdom. In Nat Commun, 2014
We identify 14 novel loci (P<5 × 10(-8)) in or near ENSA, RNU5F-1, KCNS3, AK097794, ASTN2, LHX3, CCDC91, TBX3, TRIP11, RIN3, TEKT5, LTBP4, MN1 and AP1S2, and two novel signals at known loci NPNT and GPR126, providing a basis for new understanding of the genetic determinants of these traits and pulmonary diseases in which they are altered.
Identification of gene expression-based prognostic markers in the hematopoietic stem cells of patients with myelodysplastic syndromes.
Impact
Boultwood et al., Bournemouth, United Kingdom. In J Clin Oncol, 2013
RESULTS: We identified several genes, the expression of which was significantly associated with survival of patients with MDS, including LEF1, CDH1, WT1, and MN1.
Prognostic significance of combined MN1, ERG, BAALC, and EVI1 (MEBE) expression in patients with myelodysplastic syndromes.
GeneRIF
Heuser et al., Hannover, Germany. In Ann Hematol, 2012
A high MEBE (MN1,ERG, BAALC, EVI1) expression score is an unfavorable prognostic marker in Myelodysplastic syndrome and is associated with an increased risk for progression to Acute myeloid leukemia.
Genetic and environmental risk factors for submucous cleft palate.
GeneRIF
Maier et al., Ulm, Germany. In Eur J Oral Sci, 2012
analysis of genetic variants hints at the contribution of TGFB3 and MN1 in the aetiology of submucous cleft palate
Pleiotropy and its dissection through a metabolic gene Miniature1 (Mn1) that encodes a cell wall invertase in developing seeds of maize.
GeneRIF
Cevallos-Cevallos et al., Gainesville, United States. In Plant Sci, 2012
These data provide evidence of the Mn1-dependent interconnected network of several pathways as a possible basis for pleiotropic changes in seed development.
Microdeletion del(22)(q12.2) encompassing the facial development-associated gene, MN1 (meningioma 1) in a child with Pierre-Robin sequence (including cleft palate) and neurofibromatosis 2 (NF2): a case report and review of the literature.
Review
Erdreich-Epstein et al., Los Angeles, United States. In Bmc Med Genet, 2011
FISH confirmed a deletion encompassing NF2, and chromosomal microarray identified a 3,693 kb deletion encompassing multiple genes including NF2 and MN1 (meningioma 1).Five additional patients with craniofacial dysmorphism and deletion in chromosome 22-adjacent-to or containing NF2 were identified in PubMed and the DECIPHER clinical chromosomal database.
Low expression of MN1 associates with better treatment response in older patients with de novo cytogenetically normal acute myeloid leukemia.
GeneRIF
Bloomfield et al., Columbus, United States. In Blood, 2011
low MN1 expression confers better prognosis in older CN-AML patients and may refine the European LeukemiaNet classification. Biologic features associated with MN1 expression may help identify new treatment targets.
Incidence and prognostic influence of DNMT3A mutations in acute myeloid leukemia.
Impact
Heuser et al., Hannover, Germany. In J Clin Oncol, 2011
The prognostic impact of DNMT3A mutations was evaluated in the context of other clinical prognostic markers and genetic risk factors (cytogenetic risk group; mutations in NPM1, FLT3, CEBPA, IDH1, IDH2, MLL1, NRAS, WT1, and WT1 SNPrs16754; expression levels of BAALC, ERG, EVI1, MLL5, MN1, and WT1).
Cell of origin in AML: susceptibility to MN1-induced transformation is regulated by the MEIS1/AbdB-like HOX protein complex.
Impact
Humphries et al., Vancouver, Canada. In Cancer Cell, 2011
We characterized the cell of origin and its critical pathways in MN1-induced leukemias.
MN1-ETV6 fusion gene arising from MDS with 5q-.
GeneRIF
Mecucci et al., In Leuk Res, 2011
MN1-ETV6 fusion gene arising from Myelodysplastic Syndrome with 5q trisomy is associated with acute myeloid leukemia.
Prognostic importance of histone methyltransferase MLL5 expression in acute myeloid leukemia.
Impact
Heuser et al., Hannover, Germany. In J Clin Oncol, 2011
PATIENTS AND METHODS: MLL5 transcript levels from 509 patients with AML who were treated in multicenter trials AML SHG 0199 and AML SHG 0295 and 48 healthy volunteers were analyzed by real-time reverse-transcription polymerase chain reaction in the context of other molecular markers (NPM1, FLT3, CEBPA, IDH1/IDH2, NRAS, KIT, MN1, BAALC, ERG, and WT1).
Retinoids regulate stem cell differentiation.
Review
Wagner et al., New York City, United States. In J Cell Physiol, 2011
Proteins that bind at or near RAREs include Sin3a, N-CoR1, PRAME, Trim24, NRIP1, Ajuba, Zfp423, and MN1/TEL.
Accelerated leukemogenesis by truncated CBF beta-SMMHC defective in high-affinity binding with RUNX1.
Impact
Liu et al., Bethesda, United States. In Cancer Cell, 2010
A larger pool of leukemia-initiating cells, increased MN1 expression, and retention of RUNX1 phosphorylation are potential mechanisms for accelerated leukemia development in these mice.
[Advance of study on MN1 gene in acute myeloid leukemia - review].
Review
Li et al., Nanjing, China. In Zhongguo Shi Yan Xue Ye Xue Za Zhi, 2009
The transcriptional coactivator MN1 has been identified as a gene overexpressed in certain types of human acute myeloid leukemia.
Molecular prognostic markers for adult acute myeloid leukemia with normal cytogenetics.
Review
Tse et al., Aurora, United States. In J Hematol Oncol, 2008
Molecular risk stratification for NC-AML patients may be possible due to mutations of NPM1, FLT3, MLL, and CEBPalpha as well as alterations in expression levels of BAALC, MN1, ERG, and AF1q.
The challenge of risk stratification in acute myeloid leukemia with normal karyotype.
Review
Aljurf et al., Riyadh, Saudi Arabia. In Hematol Oncol Stem Cell Ther, 2008
Emerging evidence reveals that at the submicroscopic level, AML with normal cytogenetics may carry poor prognostic genetic lesions or "molecular signatures" as is the case with FLT3 mutations and overexpression of BAALC, ERG or MN1, or may have aberrations that predict better risk as is the case with isolated NPM1 or CEBPA mutations.
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