miR-181b negatively regulates activation-induced cytidine deaminase in B cells
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C. Croce | Lin He | Laura Belver | D. Pisano | A. Ramiro | A. Villasante | V. G. de Yébenes | Susana González | Aranzazu Villasante
[1] Thomas Tuschl,et al. MicroRNA-155 is a negative regulator of activation-induced cytidine deaminase. , 2008, Immunity.
[2] Michel C Nussenzweig,et al. MicroRNA-155 suppresses activation-induced cytidine deaminase-mediated Myc-Igh translocation. , 2008, Immunity.
[3] D. Schatz,et al. Two levels of protection for the B cell genome during somatic hypermutation , 2008, Nature.
[4] A. Ramiro,et al. Oncogenic events triggered by AID, the adverse effect of antibody diversification. , 2007, Carcinogenesis.
[5] T. Ried,et al. AID-deficient Bcl-xL transgenic mice develop delayed atypical plasma cell tumors with unusual Ig/Myc chromosomal rearrangements , 2007, The Journal of experimental medicine.
[6] N. Rajewsky,et al. MiR-150 Controls B Cell Differentiation by Targeting the Transcription Factor c-Myb , 2007, Cell.
[7] M. Nussenzweig,et al. A role for AID in chromosome translocations between c-myc and the IgH variable region , 2007, The Journal of experimental medicine.
[8] M. Busslinger,et al. Life beyond cleavage: the case of Ago2 and hematopoiesis. , 2007, Genes & development.
[9] C. Sander,et al. A Mammalian microRNA Expression Atlas Based on Small RNA Library Sequencing , 2007, Cell.
[10] N. Kakazu,et al. Activation-induced cytidine deaminase (AID) promotes B cell lymphomagenesis in Emu-cmyc transgenic mice , 2007, Proceedings of the National Academy of Sciences.
[11] C. Croce,et al. MicroRNA expression and function in cancer. , 2006, Trends in molecular medicine.
[12] Stefano Volinia,et al. MicroRNA expression abnormalities in pancreatic endocrine and acinar tumors are associated with distinctive pathologic features and clinical behavior. , 2006, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[13] Anton J. Enright,et al. Zebrafish MiR-430 Promotes Deadenylation and Clearance of Maternal mRNAs , 2006, Science.
[14] Michel C. Nussenzweig,et al. Role of genomic instability and p53 in AID-induced c-myc–Igh translocations , 2006, Nature.
[15] N. Maizels. Immunoglobulin gene diversification. , 2005, Annual review of genetics.
[16] H. Horvitz,et al. MicroRNA expression profiles classify human cancers , 2005, Nature.
[17] Ralf Küppers,et al. Mechanisms of B-cell lymphoma pathogenesis , 2005, Nature Reviews Cancer.
[18] C. Burge,et al. Conserved Seed Pairing, Often Flanked by Adenosines, Indicates that Thousands of Human Genes are MicroRNA Targets , 2005, Cell.
[19] M. Nussenzweig,et al. AID Is Required for c-myc/IgH Chromosome Translocations In Vivo , 2004, Cell.
[20] Lin He,et al. MicroRNAs: small RNAs with a big role in gene regulation , 2004, Nature Reviews Genetics.
[21] Vasco M. Barreto,et al. Somatic Hypermutation Is Limited by CRM1-dependent Nuclear Export of Activation-induced Deaminase , 2004, The Journal of experimental medicine.
[22] M. Neuberger,et al. AID mutates E. coli suggesting a DNA deamination mechanism for antibody diversification , 2002, Nature.
[23] Gouri Nanjangud,et al. Hypermutation of multiple proto-oncogenes in B-cell diffuse large-cell lymphomas , 2001, Nature.
[24] T. Honjo,et al. Class Switch Recombination and Hypermutation Require Activation-Induced Cytidine Deaminase (AID), a Potential RNA Editing Enzyme , 2000, Cell.
[25] A. Fischer,et al. Activation-Induced Cytidine Deaminase (AID) Deficiency Causes the Autosomal Recessive Form of the Hyper-IgM Syndrome (HIGM2) , 2000, Cell.
[26] P. Hodgkin,et al. Switch recombination and germ-line transcription are division-regulated events in B lymphocytes. , 1999, Biochimica et biophysica acta.
[27] L. Pasqualucci,et al. AID is required for germinal center–derived lymphomagenesis , 2008, Nature Genetics.
[28] Vasco M. Barreto,et al. The role of activation-induced deaminase in antibody diversification and chromosome translocations. , 2007, Advances in immunology.
[29] Y. Pekarsky,et al. Tcl1 expression in chronic lymphocytic leukemia is regulated by miR-29 and miR-181. , 2006, Cancer research.
[30] J. Stavnezer. Antibody class switching. , 1996, Advances in immunology.