Allele‐specific loss of heterozygosity at the DAL‐1/4.1B (EPB41L3) tumor‐suppressor gene locus in the absence of mutation
暂无分享,去创建一个
Wendy A Wells | I. Newsham | L. Titus-Ernstoff | E Robert Greenberg | Linda Titus-Ernstoff | E. Greenberg | M. Mastronardi | K. Kittiniyom | Irene F Newsham | Kanokwan Kittiniyom | Michelle Mastronardi | Martha Roemer | Wendy A. Wells | Martha E Roemer | W. Wells | Kanokwan Kittiniyom
[1] D. Botstein,et al. Evidence for linkage of bipolar disorder to chromosome 18 with a parent-of-origin effect. , 1995, American journal of human genetics.
[2] I. Newsham,et al. Allelic loss on chromosome band 18p11.3 occurs early and reveals heterogeneity in breast cancer progression , 2001, Breast Cancer Research.
[3] D. Louis,et al. Multiple meningiomas: Investigating the molecular basis of sporadic and familial forms , 2003, International journal of cancer.
[4] M. Suyama,et al. Prediction of the coding sequences of unidentified human genes. XIII. The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro. , 1999, DNA research : an international journal for rapid publication of reports on genes and genomes.
[5] I. Newsham,et al. Loss of DAL-1, a protein 4.1-related tumor suppressor, is an important early event in the pathogenesis of meningiomas. , 2000, Human molecular genetics.
[6] Kyucheol Cho,et al. Frequent monoallelic deletion of PTEN and its reciprocal associatioin with PIK3CA amplification in gastric carcinoma , 2003, International journal of cancer.
[7] M. Nakao,et al. The involvement of calpain-independent proteolysis of the tumor suppressor NF2 (merlin) in schwannomas and meningiomas , 1998, Nature Medicine.
[8] J. Conboy,et al. Characterization of multiple isoforms of protein 4.1R expressed during erythroid terminal differentiation. , 1998, Blood.
[9] C. Haipek,et al. The Protein 4.1 Tumor Suppressor, DAL-1, Impairs Cell Motility, But Regulates Proliferation in a Cell-Type-Specific Fashion , 2001, Neurobiology of Disease.
[10] S. Snyder,et al. Four paralogous protein 4.1 genes map to distinct chromosomes in mouse and human. , 1998, Genomics.
[11] M. Ittmann,et al. Haploinsufficiency of the Pten tumor suppressor gene promotes prostate cancer progression , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[12] D. Cox,et al. Functional analysis of the neurofibromatosis type 2 protein by means of disease-causing point mutations. , 2000, American journal of human genetics.
[13] I. Newsham,et al. Suppression of growth and increased cellular attachment after expression of DAL‐1 in MCF‐7 breast cancer cells , 2002, International journal of cancer.
[14] I. Newsham,et al. Novel regions of allelic deletion on chromosome 18p in tumors of the lung, brain and breast , 1998, Oncogene.
[15] S. Baylin,et al. Switch from monoallelic to biallelic human IGF2 promoter methylation during aging and carcinogenesis. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[16] L. Englmeier,et al. An Alternative Domain Containing a Leucine-rich Sequence Regulates Nuclear Cytoplasmic Localization of Protein 4.1R* , 2003, The Journal of Biological Chemistry.
[17] T. Nagase,et al. Prediction of the coding sequences of unidentified human genes. XVIII. The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro. , 2000, DNA research : an international journal for rapid publication of reports on genes and genomes.
[18] O. Bogler,et al. A novel member of the NF2/ERM/4.1 superfamily with growth suppressing properties in lung cancer. , 1999, Cancer research.
[19] I. Newsham,et al. The 4.1/ezrin/radixin/moesin domain of the DAL-1/Protein 4.1B tumour suppressor interacts with 14-3-3 proteins. , 2002, The Biochemical journal.
[20] O. Ohara,et al. Type II brain 4.1 (4.1B/KIAA0987), a member of the protein 4.1 family, is localized to neuronal paranodes. , 2000, Brain research. Molecular brain research.
[21] C. Kaye,et al. Preferential loss of the paternal alleles in the 18q- syndrome. , 1997, American journal of medical genetics.
[22] O. Ohara,et al. Comparison of mRNA and protein levels of four members of the protein 4.1 family: the type II brain 4.1/4.1B/KIAA0987 is the most predominant member of the protein 4.1 family in rat brain. , 2000, Gene.
[23] F. Vitelli,et al. Analysis of the neurofibromatosis type 2 gene in different human tumors of neuroectodermal origin , 1996, Human Genetics.
[24] A. Hagemeijer,et al. Frequent NF2 gene transcript mutations in sporadic meningiomas and vestibular schwannomas. , 1994, American journal of human genetics.
[25] M. Nakao,et al. Calpain‐dependent proteolysis of NF2 protein: Involvement in schwannomas and meningiomas , 2000, Neuropathology : official journal of the Japanese Society of Neuropathology.
[26] M. Kressel,et al. Novel alternatively spliced isoforms of the neurofibromatosis type 2 tumor suppressor are targeted to the nucleus and cytoplasmic granules. , 1999, Human molecular genetics.
[27] E. Gershon,et al. Maternal inheritance and chromosome 18 allele sharing in unilineal bipolar illness pedigrees. , 1996, American journal of medical genetics.
[28] O. Ohara,et al. Molecular characterization of a new member of the protein 4.1 family (brain 4.1) in rat brain. , 1999, Brain research. Molecular brain research.
[29] D. Louis,et al. Universal absence of merlin, but not other ERM family members, in schwannomas. , 1997, The American journal of pathology.
[30] J. A. Gimm,et al. Molecular and Functional Characterization of Protein 4.1B, a Novel Member of the Protein 4.1 Family with High Level, Focal Expression in Brain* , 2000, The Journal of Biological Chemistry.
[31] J. Biegel,et al. Exon scanning for mutations of the nf2 gene in pediatric ependymomas, rhabdoid tumors and meningiomas , 1995, International journal of cancer.
[32] F. Vitelli,et al. Somatic mutations in the neurofibromatosis type 2 gene in sporadic meningiomas , 1995, Human Genetics.
[33] P. Bryant,et al. The genetics of the protein 4.1 family: organizers of the membrane and cytoskeleton. , 2000, Current opinion in cell biology.
[34] G. Kou,et al. Genomic structure of the locus encoding protein 4.1. Structural basis for complex combinational patterns of tissue-specific alternative RNA splicing. , 1993, The Journal of biological chemistry.
[35] T. Vulliamy,et al. Organization of the human protein 4.1 genomic locus: new insights into the tissue-specific alternative splicing of the pre-mRNA. , 1997, Genomics.
[36] M. Linsenmeyer,et al. DNA methylation in the promoter region of the p16 (CDKN2/MTS-1/INK4A) gene in human breast tumours , 1999, British Journal of Cancer.
[37] 木村 麗新. The involvement of calpain-dependent proteolysis of the tumor suppressor NF2 (merlin) in schwannomas and meningiomas , 1999 .
[38] B. Scheithauer,et al. Merlin, DAL‐1, and Progesterone Receptor Expression in Clinicopathologic Subsets of Meningioma: A Correlative Immunohistochemical Study of 175 Cases , 2000, Journal of neuropathology and experimental neurology.
[39] X. Estivill,et al. Predominant occurrence of somatic mutations of the NF2 gene in meningiomas and schwannomas , 1995, Genes, chromosomes & cancer.
[40] S. C. Liu,et al. The FERM domain: A unique module involved in the linkage of cytoplasmic proteins to the membrane , 1998 .
[41] D. Evans,et al. A genetic study of type 2 neurofibromatosis in the United Kingdom. I. Prevalence, mutation rate, fitness, and confirmation of maternal transmission effect on severity. , 1992, Journal of medical genetics.