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10.1128/MCB.00316-16 http://scihub22266oqcxt.onion/10.1128/MCB.00316-16 C5214850!5214850!27777312     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cell+Biol 2017 ; 37 (2): ä Nephropedia Template TP {{tp|p=27777312|t=2017. MBD4 Facilitates Immunoglobulin Class Switch Recombination |pdf=|usr=}}{{27777312}} gab.com Text MBD4 Facilitates Immunoglobulin Class Switch Recombination JO: Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27777312 #FOAvip Immunoglobulin heavy chain class switch recombination (CSR) requires targeted formation of DNA double-strand breaks (DSBs) in repetitive switch region elements followed by ligation between distal breaks. The introduction of DSBs is initiated by activation-induced cytidine deaminase (AID) and requires base excision repair (BER) and mismatch repair (MMR). The BER enzyme methyl-CpG binding domain protein 4 (MBD4) has been linked to the MMR pathway through its interaction with MutL homologue 1 (MLH1). We find that when Mbd4 exons 6 to 8 are deleted in a switching B cell line, DSB formation is severely reduced and CSR frequency is impaired. Impaired CSR can be rescued by ectopic expression of Mbd4. Mbd4 deficiency yields a deficit in DNA end processing similar to that found in MutS homologue 2 (Msh2)- and Mlh1-deficient B cells. We demonstrate that microhomology-rich S-S junctions are enriched in cells in which Mbd4 is deleted. Our studies suggest that Mbd4 is a component of MMR-directed DNA end processing. Twit Text FOAVip MBD4 Facilitates Immunoglobulin Class Switch Recombination ????Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27777312 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27777312 #FOAvip English Wikipedia <ref>{{Cite pmid|27777312}}</ref> MBD4 Facilitates Immunoglobulin Class Switch Recombination #MMPMID27777312 Grigera F; Wuerffel R; Kenter AL Mol Cell Biol 2017[Jan]; 37 (2): ä PMID27777312show ga Immunoglobulin heavy chain class switch recombination (CSR) requires targeted formation of DNA double-strand breaks (DSBs) in repetitive switch region elements followed by ligation between distal breaks. The introduction of DSBs is initiated by activation-induced cytidine deaminase (AID) and requires base excision repair (BER) and mismatch repair (MMR). The BER enzyme methyl-CpG binding domain protein 4 (MBD4) has been linked to the MMR pathway through its interaction with MutL homologue 1 (MLH1). We find that when Mbd4 exons 6 to 8 are deleted in a switching B cell line, DSB formation is severely reduced and CSR frequency is impaired. Impaired CSR can be rescued by ectopic expression of Mbd4. Mbd4 deficiency yields a deficit in DNA end processing similar to that found in MutS homologue 2 (Msh2)- and Mlh1-deficient B cells. We demonstrate that microhomology-rich S-S junctions are enriched in cells in which Mbd4 is deleted. Our studies suggest that Mbd4 is a component of MMR-directed DNA end processing. äMBD4 Facilitates Immunoglobulin Class Switch Recombination (epmc).pdf DeepDyve Pubget Overpricing