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Activation induced cytidine deaminase AID

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https://www.readbyqxmd.com/read/29665088/gain-of-function-analysis-of-cis-acting-diversification-elements-in-dt40-cells
#1
Randolph B Caldwell, Herbert Braselmann, Steffen Heuer, Ulrike Schötz, Horst Zitzelsberger
Activation-induced cytidine deaminase (AID) is required for the immunoglobulin diversification processes of somatic hypermutation, gene conversion and class-switch recombination. The targeting of AID's deamination activity is thought to be a combination of cis- and trans-acting elements, but has not been fully elucidated. Deletion analysis of putative proximal cis-regulatory motifs, while helpful, fails to identify additive versus cumulative effects, redundancy, and may create new motifs where none previously existed...
April 17, 2018: Immunology and Cell Biology
https://www.readbyqxmd.com/read/29664399/somatic-hypermutation-of-t-cell-receptor-%C3%AE-chain-contributes-to-selection-in-nurse-shark-thymus
#2
Jeannine A Ott, Caitlin D Castro, Thaddeus C Deiss, Yuko Ohta, Martin F Flajnik, Michael F Criscitiello
Since the discovery of the T cell receptor (TcR), immunologists have assigned somatic hypermutation (SHM) as a mechanism employed solely by B cells to diversify their antigen receptors. Remarkably, we found SHM acting in the thymus on α chain locus of shark TcR. SHM in developing shark T cells likely is catalyzed by activation-induced cytidine deaminase (AID) and results in both point and tandem mutations that accumulate non-conservative amino acid replacements within complementarity-determining regions (CDRs)...
April 17, 2018: ELife
https://www.readbyqxmd.com/read/29581109/b-cell-tumor-development-in-tet2-deficient-mice
#3
Enguerran Mouly, Hussein Ghamlouch, Veronique Della-Valle, Laurianne Scourzic, Cyril Quivoron, Damien Roos-Weil, Patrycja Pawlikowska, Véronique Saada, M'Boyba K Diop, Cécile K Lopez, Michaela Fontenay, Philippe Dessen, Ivo P Touw, Thomas Mercher, Said Aoufouchi, Olivier A Bernard
The TET2 gene encodes an α-ketoglutarate-dependent dioxygenase able to oxidize 5-methylcytosine into 5-hydroxymethylcytosine, which is a step toward active DNA demethylation. TET2 is frequently mutated in myeloid malignancies but also in B- and T-cell malignancies. TET2 somatic mutations are also identified in healthy elderly individuals with clonal hematopoiesis. Tet2 -deficient mouse models showed widespread hematological differentiation abnormalities, including myeloid, T-cell, and B-cell malignancies. We show here that, similar to what is observed with constitutive Tet2 -deficient mice, B-cell-specific Tet2 knockout leads to abnormalities in the B1-cell subset and a development of B-cell malignancies after long latency...
March 27, 2018: Blood Advances
https://www.readbyqxmd.com/read/29580925/macbeth-multiplex-automated-corynebacterium-glutamicum-base-editing-method
#4
Yu Wang, Ye Liu, Jiao Liu, Yanmei Guo, Liwen Fan, Xiaomeng Ni, Xiaomei Zheng, Meng Wang, Ping Zheng, Jibin Sun, Yanhe Ma
CRISPR/Cas9 or Cpf1-introduced double strand break dramatically decreases bacterial cell survival rate, which hampers multiplex genome editing in bacteria. In addition, the requirement of a foreign DNA template for each target locus is labor demanding and may encounter more GMO related regulatory hurdle in industrial applications. Herein, we developed a multiplex automated Corynebacterium glutamicum base editing method (MACBETH) using CRISPR/Cas9 and activation-induced cytidine deaminase (AID), without foreign DNA templates, achieving single-, double-, and triple-locus editing with efficiencies up to 100%, 87...
March 24, 2018: Metabolic Engineering
https://www.readbyqxmd.com/read/29545328/genetic-landscape-of-hepatitis-b-virus-associated-diffuse-large-b-cell-lymphoma
#5
Weicheng Ren, Xiaofei Ye, Hong Su, Wei Li, Dongbing Liu, Mohammad Pirmoradian, Xianhuo Wang, Bo Zhang, Qiang Zhang, Longyun Chen, Man Nie, Yao Liu, Bin Meng, Huiqiang Huang, Wenqi Jiang, Yixin Zeng, Wenyu Li, Kui Wu, Yong Hou, Klas G Wiman, Zhiming Li, Huilai Zhang, Roujun Peng, Shida Zhu, Qiang Pan-Hammarström
Hepatitis B virus (HBV) infection is endemic in some parts of Asia, Africa and South America and remains to be a significant public health problem in these areas. It is known as a leading risk factor for the development of hepatocellular carcinoma, but epidemiological studies have also shown that the infection may increase the incidence of several types B-cell lymphoma. Here, by characterizing altogether 275 Chinese diffuse large B-cell lymphoma (DLBCL) patients, we showed that patients with concomitant HBV infection (surface antigen positive, HBsAg+ ) are characterized by a younger age, a more advanced disease stage at diagnosis and a reduced overall survival...
March 15, 2018: Blood
https://www.readbyqxmd.com/read/29541074/pten-regulated-aid-transcription-in-germinal-center-b-cells-is-essential-for-the-class-switch-recombination-and-igg-antibody-responses
#6
Jing Wang, Sichen Liu, Baidong Hou, Meixiang Yang, Zhongjun Dong, Hai Qi, Wanli Liu
Class-switch recombination (CSR) and somatic hypermutation (SHM) occur during the differentiation of germinal center B cells (GCBs). Activation-induced cytidine deaminase (AID) is responsible for both CSR and SHM in GCBs. Here, we show that ablation of PTEN through the Cγ1-Cre mediated recombination significantly influences the CSR and SHM responses. The GCs fail to produce the IgG1 B cells, the high affinity antibodies and nearly lost the dark zone (DZ) in Ptenfl/fl Cγ1Cre/+ mice after immunization, suggesting the impaired GC structure...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29535729/epigenomic-modifications-mediating-antibody-maturation
#7
REVIEW
Emily C Sheppard, Rikke Brandstrup Morrish, Michael J Dillon, Rebecca Leyland, Richard Chahwan
Epigenetic modifications, such as histone modifications, DNA methylation status, and non-coding RNAs (ncRNA), all contribute to antibody maturation during somatic hypermutation (SHM) and class-switch recombination (CSR). Histone modifications alter the chromatin landscape and, together with DNA primary and tertiary structures, they help recruit Activation-Induced Cytidine Deaminase (AID) to the immunoglobulin (Ig) locus. AID is a potent DNA mutator, which catalyzes cytosine-to-uracil deamination on single-stranded DNA to create U:G mismatches...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29511621/robust-dna-repair-in-paxx-deficient-mammalian-cells
#8
Alisa Dewan, Mengtan Xing, Marie Benner Lundbæk, Raquel Gago-Fuentes, Carole Beck, Per Arne Aas, Nina-Beate Liabakk, Siri Sæterstad, Khac Thanh Phong Chau, Bodil Merete Kavli, Valentyn Oksenych
To ensure genome stability, mammalian cells employ several DNA repair pathways. Nonhomologous DNA end joining (NHEJ) is the DNA repair process that fixes double-strand breaks throughout the cell cycle. NHEJ is involved in the development of B and T lymphocytes through its function in V(D)J recombination and class switch recombination (CSR). NHEJ consists of several core and accessory factors, including Ku70, Ku80, XRCC4, DNA ligase 4, DNA-PKcs, Artemis, and XLF. Paralog of XRCC4 and XLF (PAXX) is the recently described accessory NHEJ factor that structurally resembles XRCC4 and XLF and interacts with Ku70/Ku80...
March 2018: FEBS Open Bio
https://www.readbyqxmd.com/read/29472448/double-stranded-dna-break-polarity-skews-repair-pathway-choice-during-intrachromosomal-and-interchromosomal-recombination
#9
Alexanda K Ling, Clare C So, Michael X Le, Audrey Y Chen, Lisa Hung, Alberto Martin
Activation-induced cytidine deaminase (AID) inflicts DNA damage at Ig genes to initiate class switch recombination (CSR) and chromosomal translocations. However, the DNA lesions formed during these processes retain an element of randomness, and thus knowledge of the relationship between specific DNA lesions and AID-mediated processes remains incomplete. To identify necessary and sufficient DNA lesions in CSR, the Cas9 endonuclease and nickase variants were used to program DNA lesions at a greater degree of predictability than is achievable with conventional induction of CSR...
February 22, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29427373/advanced-cirrhosis-drives-enhanced-b-cell-differentiation-resulting-in-hyperglobulinemia
#10
Hiroyoshi Doi, Eiichi Hayashi, Jun Arai, Masayuki Tojo, Kenichi Morikawa, Junichi Eguchi, Takayoshi Ito, Tatsuya Kanto, David E Kaplan, Hitoshi Yoshida
BACKGROUND AND AIM: The mechanism underlying hyperglobulinemia in cirrhosis, a long appreciated phenomenon, has never been clearly understood. The aim of this study is to investigate the basis for changes in humoral immunity observed in cirrhosis. METHODS: We retrospectively reviewed our medical record to analyze serum immunoglobulin levels in patients with liver disease. We also prospectively analyzed peripheral blood mononuclear cells (PBMC) and sera from liver disease patients...
February 10, 2018: Journal of Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/29388096/activation-induced-cytidine-deaminase-aided-in-vitro-antibody-evolution
#11
Lili An, Chuan Chen, Ruiqi Luo, Yun Zhao, Haiying Hang
Activation-induced cytidine deaminase (AID) initiates somatic hypermutation (SHM) by converting deoxycytidines (dC) to deoxyuracils (dU) which then can induce other mutations, and plays a central role in introducing diversification of the antibody repertoire in B cells. Ectopic expression of AID in bacteria and non-B cells can also lead to frequent mutations in highly expressed genes. Taking advantage of this feature of AID, in recent years, systems coupling in vitro somatic hypermutation and mammalian cell surface display have been developed, with unique benefits in antibody discovery and optimization in vitro...
2018: Methods in Molecular Biology
https://www.readbyqxmd.com/read/29343743/expression-and-subcellular-localisation-of-aid-and-apobec3-in-adenoid-and-palatine-tonsils
#12
Noriko Seishima, Satoru Kondo, Kousho Wakae, Naohiro Wakisaka, Eiji Kobayashi, Makoto Kano, Makiko Moriyama-Kita, Yosuke Nakanishi, Kazuhira Endo, Tomoko Imoto, Kazuya Ishikawa, Hisashi Sugimoto, Miyako Hatano, Takayoshi Ueno, Miki Koura, Koichi Kitamura, Masamichi Muramatsu, Tomokazu Yoshizaki
Activation-induced cytidine deaminase (AID) and apolipoprotein B mRNA-editing catalytic polypeptide 3 (A3) family are cytidine deaminases that play critical roles in B-cell maturation, antiviral immunity and carcinogenesis. Adenoids and palatine tonsils are secondary lymphoid immune organs, in which AID and A3s are thought to have several physiological or pathological roles. However, the expression of AID or A3s in these organs has not been investigated. Therefore, we investigated the expression profiles of AID and A3s, using 67 samples of adenoids and palatine tonsils from patients, with reverse transcription quantitative polymerase chain reaction (RT-qPCR) and immunohistochemical analyses...
January 17, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29321370/activation-induced-cytidine-deaminase-deficiency-accelerates-autoimmune-diabetes-in-nod-mice
#13
Qiyuan Tan, Ningwen Tai, Yangyang Li, James Pearson, Sean Pennetti, Zhiguang Zhou, F Susan Wong, Li Wen
B cells play an important role in type 1 diabetes (T1D) development. However, the role of B cell activation-induced cytidine deaminase (AID) in diabetes development is not clear. We hypothesized that AID is important in the immunopathogenesis of T1D. To test this hypothesis, we generated AID-deficient (AID-/-) NOD mice. We found that AID-/-NOD mice developed accelerated T1D, with worse insulitis and high levels of anti-insulin autoantibody in the circulation. Interestingly, neither maternal IgG transferred through placenta, nor IgA transferred through milk affected the accelerated diabetes development...
January 11, 2018: JCI Insight
https://www.readbyqxmd.com/read/29251015/prognostic-impact-of-activation-induced-cytidine-deaminase-expression-for-patients-with-diffuse-large-b-cell-lymphoma
#14
Hiroshi Arima, Masakazu Fujimoto, Momoko Nishikori, Toshiyuki Kitano, Wataru Kishimoto, Masakatsu Hishizawa, Tadakazu Kondo, Kouhei Yamashita, Masahiro Hirata, Hironori Haga, Akifumi Takaori-Kondo
Activation-induced cytidine deaminase (AID) plays important roles in the development of diffuse large B-cell lymphoma (DLBCL); however, its prognostic value remains controversial. Here, we evaluated AID expression in 71 DLBCL patients treated with R-CHOP by immunohistochemistry and investigated its prognostic significance. AID expression was detected in 40.8% of DLBCL samples and associated with IRF4 expression. Notably, AID expression correlated with shorter progression-free survival and overall survival for patients with high (3-5) international prognostic index (IPI) score...
December 18, 2017: Leukemia & Lymphoma
https://www.readbyqxmd.com/read/29199976/hydrogen-bonds-are-a-primary-driving-force-for-de-novo-protein-folding
#15
Schuyler Lee, Chao Wang, Haolin Liu, Jian Xiong, Renee Jiji, Xia Hong, Xiaoxue Yan, Zhangguo Chen, Michal Hammel, Yang Wang, Shaodong Dai, Jing Wang, Chengyu Jiang, Gongyi Zhang
The protein-folding mechanism remains a major puzzle in life science. Purified soluble activation-induced cytidine deaminase (AID) is one of the most difficult proteins to obtain. Starting from inclusion bodies containing a C-terminally truncated version of AID (residues 1-153; AID153 ), an optimized in vitro folding procedure was derived to obtain large amounts of AID153 , which led to crystals with good quality and to final structural determination. Interestingly, it was found that the final refolding yield of the protein is proline residue-dependent...
December 1, 2017: Acta Crystallographica. Section D, Structural Biology
https://www.readbyqxmd.com/read/29188055/aberrant-expression-of-interleukin-10-and-activation-induced-cytidine-deaminase-in-b-cells-from-patients-with-beh%C3%A3-et-s-disease
#16
Jeong-Yun Yoon, Yeojin Lee, Seong-Lan Yu, Hee-Kyung Yoon, Ha-Yan Park, Chung-Il Joung, Seok-Rae Park, Mihye Kwon, Jaeku Kang
Despite extensive studies, the pathogenesis of Behçet's disease (BD) remains unclear. In particular, the roles of B cells in patients with BD have not been elucidated. Activation-induced cytidine deaminase (AID) is a critical enzyme for immunoglobulin (Ig) heavy chain class switching and somatic hypermutation in B cells and the abnormal expression of AID in various immune conditions has previously been studied. B10 cells, an interleukin (IL)-10-secreting subset of regulatory B cells, function to downregulate inflammation and autoimmunity...
December 2017: Biomedical Reports
https://www.readbyqxmd.com/read/29161581/dna-rna-hybrid-substrates-modulate-the-catalytic-activity-of-purified-aid
#17
COMPARATIVE STUDY
Hala S Abdouni, Justin J King, Atefeh Ghorbani, Heather Fifield, Lesley Berghuis, Mani Larijani
Activation-induced cytidine deaminase (AID) converts cytidine to uridine at Immunoglobulin (Ig) loci, initiating somatic hypermutation and class switching of antibodies. In vitro, AID acts on single stranded DNA (ssDNA), but neither double-stranded DNA (dsDNA) oligonucleotides nor RNA, and it is believed that transcription is the in vivo generator of ssDNA targeted by AID. It is also known that the Ig loci, particularly the switch (S) regions targeted by AID are rich in transcription-generated DNA/RNA hybrids...
January 2018: Molecular Immunology
https://www.readbyqxmd.com/read/29158395/histone-methyltransferase-mmset-promotes-aid-mediated-dna-breaks-at-the-donor-switch-region-during-class-switch-recombination
#18
Hai Vu Nguyen, Junchao Dong, Rohit A Panchakshari, Vipul Kumar, Frederick W Alt, Jean-Christophe Bories
In B cells, Ig class switch recombination (CSR) is initiated by activation-induced cytidine deaminase (AID), the activity of which leads to DNA double-strand breaks (DSBs) within IgH switch (S) regions. Preferential targeting of AID-mediated DSBs to S sequences is critical for allowing diversification of antibody functions, while minimizing potential off-target oncogenic events. Here, we used gene targeted inactivation of histone methyltransferase (HMT) multiple myeloma SET domain (MMSET) in mouse B cells and the CH12F3 cell line to explore its role in CSR...
December 5, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29136157/depletion-of-recombination-specific-cofactors-by-the-c-terminal-mutant-of-the-activation-induced-cytidine-deaminase-causes-the-dominant-negative-effect-on-class-switch-recombination
#19
Azza Al Ismail, Afzal Husain, Maki Kobayashi, Tasuku Honjo, Nasim A Begum
Activation-induced cytidine deaminase (AID) is essential for class-switch recombination (CSR) and somatic hypermutation (SHM) of immunoglobulin genes. Studies on in vitro mutagenized AID as well as its mutations in human patients with hyper-IgM (HIGM)-syndrome type II revealed that C-terminal AID mutations were defective in CSR whereas their DNA cleavage and SHM activities remained intact. The C-terminal mutants of AID were speculated to exert the dominant negative effect on wild-type (WT) AID whereas its mechanism remains unknown...
December 30, 2017: International Immunology
https://www.readbyqxmd.com/read/29122947/phosphorylation-promotes-activation-induced-cytidine-deaminase-activity-at-the-myc-oncogene
#20
Yunxiang Mu, Monika A Zelazowska, Kevin M McBride
Activation-induced cytidine deaminase (AID) is a mutator enzyme that targets immunoglobulin (Ig) genes to initiate antibody somatic hypermutation (SHM) and class switch recombination (CSR). Off-target AID association also occurs, which causes oncogenic mutations and chromosome rearrangements. However, AID occupancy does not directly correlate with DNA damage, suggesting that factors beyond AID association contribute to mutation targeting. CSR and SHM are regulated by phosphorylation on AID serine38 (pS38), but the role of pS38 in off-target activity has not been evaluated...
December 4, 2017: Journal of Experimental Medicine
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