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Artykuły w czasopismach na temat „Recombination activating genes”

Autor: Grafiati

Data publikacji: 6 września 2023

Data aktualizacji: 31 lipca 2025

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1

Haines, Brian B., Chun Jeih Ryu, and Jianzhu Chen. "Recombination Activating Genes (RAG) in Lymphoma Development." Cell Cycle 5, no. 9 (2006): 913–16. http://dx.doi.org/10.4161/cc.5.9.2732.

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Panchin, Yuri, and Leonid L. Moroz. "Molluscan mobile elements similar to the vertebrate Recombination-Activating Genes." Biochemical and Biophysical Research Communications 369, no. 3 (2008): 818–23. http://dx.doi.org/10.1016/j.bbrc.2008.02.097.

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Lamb, Teresa M., and Aaron P. Mitchell. "Coupling of Saccharomyces cerevisiae Early Meiotic Gene Expression to DNA Replication Depends Upon RPD3 and SIN3." Genetics 157, no. 2 (2001): 545–56. http://dx.doi.org/10.1093/genetics/157.2.545.

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Abstract It has been established that meiotic recombination and chromosome segregation are inhibited when meiotic DNA replication is blocked. Here we demonstrate that early meiotic gene (EMG) expression is also inhibited by a block in replication. Since early meiotic genes are required to promote meiotic recombination and DNA division, the low expression of these genes may contribute to the block in meiotic progression. We have identified three Hur– (HU reduced recombination) mutants that fail to couple meiotic recombination and gene expression with replication. One of these mutations is in RP

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4

Li, Tong-Tong, Shuhua Han, Mike Cubbage, and Biao Zheng. "Continued expression of recombination-activating genes and TCR gene recombination in human peripheral T cells." European Journal of Immunology 32, no. 10 (2002): 2792–99. http://dx.doi.org/10.1002/1521-4141(2002010)32:10<2792::aid-immu2792>3.0.co;2-i.

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5

Yannoutsos, Nikos, Patrick Wilson, Wong Yu, et al. "The Role of Recombination Activating Gene (RAG) Reinduction in Thymocyte Development in Vivo." Journal of Experimental Medicine 194, no. 4 (2001): 471–80. http://dx.doi.org/10.1084/jem.194.4.471.

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Assembly of T cell receptor (TCR)α/β genes by variable/diversity/joining (V[D]J) rearrangement is an ordered process beginning with recombination activating gene (RAG) expression and TCRβ recombination in CD4−CD8−CD25+ thymocytes. In these cells, TCRβ expression leads to clonal expansion, RAG downregulation, and TCRβ allelic exclusion. At the subsequent CD4+CD8+ stage, RAG expression is reinduced and V(D)J recombination is initiated at the TCRα locus. This second wave of RAG expression is terminated upon expression of a positively selected α/β TCR. To examine the physiologic role of the second

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6

Ohmori, Hitoshi, та Masaki Hikida. "Expression and Function of Recombination Activating Genes in Mature В Cells". Critical Reviews™ in Immunology 18, № 3 (1998): 221–35. http://dx.doi.org/10.1615/critrevimmunol.v18.i3.30.

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7

Gennery, Andrew R., Elizabeth Hodges, Anthony P. Williams, et al. "Omenn's syndrome occurring in patients without mutations in recombination activating genes." Clinical Immunology 116, no. 3 (2005): 246–56. http://dx.doi.org/10.1016/j.clim.2005.04.014.

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8

Tsai, Albert G., and Michael R. Lieber. "RAGs found “not guilty”: cleared by DNA evidence." Blood 111, no. 4 (2008): 1750. http://dx.doi.org/10.1182/blood-2007-09-113381.

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A recent paper from the Alt laboratory shows that recombination activating genes (RAGs) are not responsible for double-strand DNA breaks associated with some chromosomal translocations in pre–T-cell lymphomas.

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9

Jessen, Jason R., Tammy N. Jessen, Steven S. Vogel, and Shuo Lin. "Concurrent expression of recombination activating genes 1 and 2 in zebrafish olfactory sensory neurons." genesis 29, no. 4 (2001): 156–62. http://dx.doi.org/10.1002/gene.1019.

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10

Oltz, E. M., F. W. Alt, W. C. Lin, et al. "A V(D)J recombinase-inducible B-cell line: role of transcriptional enhancer elements in directing V(D)J recombination." Molecular and Cellular Biology 13, no. 10 (1993): 6223–30. http://dx.doi.org/10.1128/mcb.13.10.6223-6230.1993.

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Rapid analysis of mechanisms that regulate V(D)J recombination has been hampered by the lack of appropriate cell systems that reproduce aspects of normal prelymphocyte physiology in which the recombinase is activated, accessible antigen receptor loci are rearranged, and rearrangement status is fixed by termination of recombinase expression. To generate such a system, we introduced heat shock-inducible V(D)J recombination-activating genes (RAG) 1 and 2 into a recombinationally inert B-cell line. Heat shock treatment of these cells rapidly induced high levels of RAG transcripts and RAG proteins

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11

Oltz, E. M., F. W. Alt, W. C. Lin, et al. "A V(D)J recombinase-inducible B-cell line: role of transcriptional enhancer elements in directing V(D)J recombination." Molecular and Cellular Biology 13, no. 10 (1993): 6223–30. http://dx.doi.org/10.1128/mcb.13.10.6223.

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Rapid analysis of mechanisms that regulate V(D)J recombination has been hampered by the lack of appropriate cell systems that reproduce aspects of normal prelymphocyte physiology in which the recombinase is activated, accessible antigen receptor loci are rearranged, and rearrangement status is fixed by termination of recombinase expression. To generate such a system, we introduced heat shock-inducible V(D)J recombination-activating genes (RAG) 1 and 2 into a recombinationally inert B-cell line. Heat shock treatment of these cells rapidly induced high levels of RAG transcripts and RAG proteins

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12

Thwaites, Daniel T., Clive Carter, Dylan Lawless, Sinisa Savic, and Joan M. Boyes. "A novel RAG1 mutation reveals a critical in vivo role for HMGB1/2 during V(D)J recombination." Blood 133, no. 8 (2019): 820–29. http://dx.doi.org/10.1182/blood-2018-07-866939.

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Abstract The Recombination Activating Genes, RAG1 and RAG2, are essential for V(D)J recombination and adaptive immunity. Mutations in these genes often cause immunodeficiency, the severity of which reflects the importance of the altered residue or residues during recombination. Here, we describe a novel RAG1 mutation that causes immunodeficiency in an unexpected way: The mutated protein severely disrupts binding of the accessory protein, HMGB1. Although HMGB1 enhances RAG cutting in vitro, its role in vivo was controversial. We show here that reduced HMGB1 binding by the mutant protein dramati

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13

Goebel, Peter, Noel Janney, Joaquín R. Valenzuela, William J. Romanow, Cornelis Murre, and Ann J. Feeney. "Localized Gene-Specific Induction of Accessibility to V(D)j Recombination Induced by E2a and Early B Cell Factor in Nonlymphoid Cells." Journal of Experimental Medicine 194, no. 5 (2001): 645–56. http://dx.doi.org/10.1084/jem.194.5.645.

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Accessibility of immunoglobulin (Ig) gene segments to V(D)J recombination is highly regulated and is normally only achieved in B cell precursors. We previously showed that ectopic expression of E2A or early B cell factor (EBF) with recombination activating gene (RAG) induces rearrangement of IgH and IgL genes in nonlymphoid cells. VκI genes throughout the locus were induced to rearrange after transfection with E2A, suggesting that the entire Vκ locus was accessible. However, here we show that Ig loci are not opened globally but that recombination is localized. Gene families are interspersed in

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14

Nagawa, Fumikiyo, Masami Kodama, Tadashi Nishihara, Kei-ichiro Ishiguro, and Hitoshi Sakano. "Footprint Analysis of Recombination Signal Sequences in the 12/23 Synaptic Complex of V(D)J Recombination." Molecular and Cellular Biology 22, no. 20 (2002): 7217–25. http://dx.doi.org/10.1128/mcb.22.20.7217-7225.2002.

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ABSTRACT In V(D)J joining of antigen receptor genes, two recombination signal sequences (RSSs), 12-RSS and 23-RSS, are paired and complexed with the protein products of recombination-activating genes RAG1 and RAG2. Using magnetic beads, we purified the pre- and postcleavage complexes of V(D)J joining and analyzed them by DNase I footprinting. In the precleavage synaptic complex, strong protection was seen not only in the 9-mer and spacer regions but also near the coding border of the 7-mer. This is a sharp contrast to the single RSS-RAG complex where the 9-mer plays a major role in the interac

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15

Knecht, Hans, Pierre Brousset, Edith Bachmann, Gorm Pallesen, and Bernhard F. Odermatt. "Expression of Human Recombination Activating Genes (RAG-1 and RAG-2) in Lymphoma." Leukemia & Lymphoma 15, no. 5-6 (1994): 399–403. http://dx.doi.org/10.3109/10428199409049742.

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16

Amin, Rupesh H., and Mark S. Schlissel. "Foxo1 directly regulates the transcription of recombination-activating genes during B cell development." Nature Immunology 9, no. 6 (2008): 613–22. http://dx.doi.org/10.1038/ni.1612.

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17

Willett, Catherine E., Jason J. Cherry, and Lisa A. Steiner. "Characterization and expression of the recombination activating genes (rag1 and rag2) of zebrafish." Immunogenetics 45, no. 6 (1997): 394–404. http://dx.doi.org/10.1007/s002510050221.

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18

Fuschiotti, Patrizia, Nagaradona Harindranath, Rose G. Mage, Wayne T. McCormack, Pushparani Dhanarajan, and Kenneth H. Roux. "Recombination activating genes-1 and -2 of the rabbit: Cloning and characterization of germline and expressed genes." Molecular Immunology 30, no. 11 (1993): 1021–32. http://dx.doi.org/10.1016/0161-5890(93)90127-w.

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19

Kuhn-Hallek, I., DR Sage, L. Stein, H. Groelle, and JD Fingeroth. "Expression of recombination activating genes (RAG-1 and RAG-2) in Epstein-Barr virus-bearing B cells [see comments]." Blood 85, no. 5 (1995): 1289–99. http://dx.doi.org/10.1182/blood.v85.5.1289.bloodjournal8551289.

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Recombination activating genes 1 and 2 (RAG-1 and RAG-2), are the only lymphoid-specific genes required for the site-directed recombination reaction leading to generation of B-cell receptors and T-cell receptors (TCRs). RAGs are normally expressed during a narrow window of precursor lymphocyte development. RAG expression was examined in Epstein-Barr virus (EBV)-infected B cells. No steady-state RAG RNA was found in EBV immortalized cells, including newly established B lymphoblastoid cell lines derived from precursor lymphocytes that transcribed RAGs at the time of infection. RAG RNAs were dete

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20

Kim, Keun-Yong, Myeong-Hun Ko, Huanzhang Liu, et al. "Phylogenetic Relationships ofPseudorasbora,Pseudopungtungia, andPungtungia(Teleostei; Cypriniformes; Gobioninae) Inferred from Multiple Nuclear Gene Sequences." BioMed Research International 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/347242.

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Gobionine species belonging to the generaPseudorasbora,Pseudopungtungia, andPungtungia(Teleostei; Cypriniformes; Cyprinidae) have been heavily studied because of problems on taxonomy, threats of extinction, invasion, and human health. Nucleotide sequences of three nuclear genes, that is, recombination activating protein gene 1 (rag1), recombination activating gene 2 (rag2), and early growth response 1 gene (egr1), fromPseudorasbora,Pseudopungtungia, andPungtungiaspecies residing in China, Japan, and Korea, were analyzed to elucidate their intergeneric and interspecific phylogenetic relationshi

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21

Gennery, Andrew. "Recent advances in understanding RAG deficiencies." F1000Research 8 (February 4, 2019): 148. http://dx.doi.org/10.12688/f1000research.17056.1.

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Recombination-activating genes (RAG)1 and RAG2 initiate the molecular processes that lead to lymphocyte receptor formation through VDJ recombination. Nonsense mutations in RAG1/RAG2 cause the most profound immunodeficiency syndrome, severe combined immunodeficiency (SCID). Other severe and less-severe clinical phenotypes due to mutations in RAG genes are now recognized. The degree of residual protein function may permit some lymphocyte receptor formation, which confers a less-severe clinical phenotype. Many of the non-SCID phenotypes are associated with autoimmunity. New findings into the effe

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22

Lange, Miles, Wanqin Xie, Sang Yong Hong, et al. "The V(D)J recombination machinery is associated with the nuclear matrix (88.3)." Journal of Immunology 184, no. 1_Supplement (2010): 88.3. http://dx.doi.org/10.4049/jimmunol.184.supp.88.3.

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Abstract Somatic recombination of immunoglobulin or T cell antigen receptor genes occurs through recombination activating gene product (RAG)-mediated cleavage at recombination signal sequences (RSS) and subsequently, the broken DNA ends are repaired by non-homologue end joining (NHEJ) enzymes. Here, we show that RAG1, RAG2, and many NHEJ factors in B lineage cells are associated with the nuclear matrix. The core RAG1 and RAG2 proteins have their own nuclear matrix targeting regions. RAG-mediated double stranded DNA breaks at the Jκ4 RSS can be readily detected in the nuclear matrix fraction in

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23

He, Youdi, Ning Ma, He Xiao, et al. "B cell activating factor (BAFF) induces the transcription of recombination-activating genes in transitional stage 1 B cells." Central European Journal of Immunology 3 (2013): 336–42. http://dx.doi.org/10.5114/ceji.2013.37758.

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24

ZOU, Hong-yun, Li MA, Min-jie MENG, et al. "Expression of recombination-activating genes and T cell receptor gene recombination in the human T cell leukemia cell line." Chinese Medical Journal 120, no. 5 (2007): 410–15. http://dx.doi.org/10.1097/00029330-200703010-00013.

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25

Livak, F., and D. G. Schatz. "T-cell receptor alpha locus V(D)J recombination by-products are abundant in thymocytes and mature T cells." Molecular and Cellular Biology 16, no. 2 (1996): 609–18. http://dx.doi.org/10.1128/mcb.16.2.609.

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In addition to the assembled coding regions of immunoglobulin and T-cell receptor (TCR) genes, the V(D)J recombination reaction can in principle generate three types of by-products in normal developing lymphocytes: broken DNA molecules that terminate in a recombination signal sequence or a coding region (termed signal or coding end molecules, respectively) and DNA molecules containing fused recombination signal sequences (termed reciprocal products). Using a quantitative Southern blot analysis of the murine TCR alpha locus, we demonstrate that substantial amounts of signal end molecules and re

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26

Yoshikawa, Genki, Kazuko Miyazaki, Hiroyuki Ogata, and Masaki Miyazaki. "The Evolution of Rag Gene Enhancers and Transcription Factor E and Id Proteins in the Adaptive Immune System." International Journal of Molecular Sciences 22, no. 11 (2021): 5888. http://dx.doi.org/10.3390/ijms22115888.

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Adaptive immunity relies on the V(D)J DNA recombination of immunoglobulin (Ig) and T cell receptor (TCR) genes, which enables the recognition of highly diverse antigens and the elicitation of antigen-specific immune responses. This process is mediated by recombination-activating gene (Rag) 1 and Rag2 (Rag1/2), whose expression is strictly controlled in a cell type-specific manner; the expression of Rag1/2 genes represents a hallmark of lymphoid lineage commitment. Although Rag genes are known to be evolutionally conserved among jawed vertebrates, how Rag genes are regulated by lineage-specific

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Wayne, J., H. Suh, K. A. Sokol, et al. "TCR selection and allelic exclusion in RAG transgenic mice that exhibit abnormal T cell localization in lymph nodes and lymphatics." Journal of Immunology 153, no. 12 (1994): 5491–502. http://dx.doi.org/10.4049/jimmunol.153.12.5491.

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Abstract RAG-1 and RAG-2 are developmentally regulated genes that are essential for V(D)J recombination and lymphocyte development. Expression of RAG-1 and RAG-2 by thymocytes is normally limited to cells that have not completed selection. We have previously documented that persistent expression of the recombinase activating genes (RAG) in transgenic mice results in aberrant thymic development, altered lymphatic microanatomy, and a profound immunodeficiency. Here we further document the pathologic changes found in TG.RAG-1,2 mice and examine the role of TCR recombination and positive and negat

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Dorsett, Yair, Davide F. Robbiani, Mila Jankovic, Bernardo Reina-San-Martin, Thomas R. Eisenreich, and Michel C. Nussenzweig. "A role for AID in chromosome translocations between c-myc and the IgH variable region." Journal of Experimental Medicine 204, no. 9 (2007): 2225–32. http://dx.doi.org/10.1084/jem.20070884.

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Chromosome translocations between oncogenes and the region spanning the immunoglobulin (Ig) heavy chain (IgH) variable (V), diversity (D), and joining (J) gene segments (Ig V-JH region) are found in several mature B cell lymphomas in humans and mice. The breakpoints are frequently adjacent to the recombination signal sequences targeted by recombination activating genes 1 and 2 during antigen receptor assembly in pre–B cells, suggesting that these translocations might be the result of aberrant V(D)J recombination. However, in mature B cells undergoing activation-induced cytidine deaminase (AID)

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29

Thomson, Daniel, Hezrin Shahrin, Paul Wang, et al. "High Recombination Activating Gene (RAG) Expression and RAG Mediated Recombination Is Associated with Oncogenic Rearrangement Observed with Tyrosine Kinase Inhibitor Resistant CML." Blood 132, Supplement 1 (2018): 3001. http://dx.doi.org/10.1182/blood-2018-99-111212.

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Abstract Background Patients with chronic myeloid leukemia (CML) who develop blast crisis are resistant to TKI therapy. A key focus in CML research is the identification of genetic factors that promote blast crisis and TKI resistance. By using an integrative genomic approach we recently reported frequent structural variation in CML patients, particularly at lymphoid blast crisis (LBC) (Blood, 2018). Developing lymphocytes are uniquely equipped with a molecular toolkit capable of programmed DNA damage and structural variant formation; the V(D)J recombination pathway. Recombination activating ge

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30

HILLION, SOPHIE, CAROLINE ROCHAS, PIERRE YOUINOU, and CHRISTOPHE JAMIN. "Expression and Reexpression of Recombination Activating Genes: Relevance to the Development of Autoimmune States." Annals of the New York Academy of Sciences 1050, no. 1 (2005): 10–18. http://dx.doi.org/10.1196/annals.1313.002.

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Knecht, H., DJ Joske, A. Emery-Goodman, E. Bachmann, F. Bachmann, and BF Odermatt. "Expression of human recombination activating genes (RAG-1 and RAG-2) in Hodgkin's disease." Blood 80, no. 11 (1992): 2867–72. http://dx.doi.org/10.1182/blood.v80.11.2867.2867.

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Abstract The differentiation status of Sternberg-Reed (SR) cells is still not well defined, primarily because of their scarcity in tumor biopsies of Hodgkin's disease (HD). In this study we have determined the genomic differentiation status of SR cells by quantitation of recombinase activating gene (RAG) expression. RAG genes are selectively transcribed in immature lymphoid cells. In B cells they are silent after genomic rearrangement has occurred, whereas in T cells they are downregulated during positive selection of double-positive thymocytes into single- positive cells. RNA from tumor biops

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Knecht, H., DJ Joske, A. Emery-Goodman, E. Bachmann, F. Bachmann, and BF Odermatt. "Expression of human recombination activating genes (RAG-1 and RAG-2) in Hodgkin's disease." Blood 80, no. 11 (1992): 2867–72. http://dx.doi.org/10.1182/blood.v80.11.2867.bloodjournal80112867.

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The differentiation status of Sternberg-Reed (SR) cells is still not well defined, primarily because of their scarcity in tumor biopsies of Hodgkin's disease (HD). In this study we have determined the genomic differentiation status of SR cells by quantitation of recombinase activating gene (RAG) expression. RAG genes are selectively transcribed in immature lymphoid cells. In B cells they are silent after genomic rearrangement has occurred, whereas in T cells they are downregulated during positive selection of double-positive thymocytes into single- positive cells. RNA from tumor biopsies eithe

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33

Nishana, Mayilaadumveettil, and Sathees C. Raghavan. "Role of recombination activating genes in the generation of antigen receptor diversity and beyond." Immunology 137, no. 4 (2012): 271–81. http://dx.doi.org/10.1111/imm.12009.

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Hikida, M., M. Mori, T. Kawabata, T. Takai, and H. Ohmori. "Characterization of B cells expressing recombination activating genes in germinal centers of immunized mouse lymph nodes." Journal of Immunology 158, no. 6 (1997): 2509–12. http://dx.doi.org/10.4049/jimmunol.158.6.2509.

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Abstract Products of recombination activating genes (RAG-1 and RAG-2) involved in the rearrangement of Ig genes have been shown to be expressed only in immature stages of B cells. However, we have recently found that RAG genes were re-expressed in mature mouse B cells activated in vitro and in germinal centers (GCs) of immunized mouse lymph nodes (LNs). Here, we report that RAG transcripts and their proteins were expressed in parallel with the formation of GCs in popliteal LNs from mice immunized in the hind footpads. Immunocytochemical analysis revealed that RAG+ B cells were localized within

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35

Thorey, Irmgard S., Katrin Muth, Andreas P. Russ, Jürgen Otte, Armin Reffelmann, and Harald von Melchner. "Selective Disruption of Genes Transiently Induced in Differentiating Mouse Embryonic Stem Cells by Using Gene Trap Mutagenesis and Site-Specific Recombination." Molecular and Cellular Biology 18, no. 5 (1998): 3081–88. http://dx.doi.org/10.1128/mcb.18.5.3081.

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ABSTRACT A strategy employing gene trap mutagenesis and site-specific recombination (Cre/loxP) has been used to identify genes that are transiently expressed during early mouse development. Embryonic stem cells expressing a reporter plasmid that codes for neomycin phosphotransferase and Escherichia coli LacZ were infected with a retroviral gene trap vector (U3Cre) carrying coding sequences for Cre recombinase (Cre) in the U3 region. Activation of Cre expression from integrations into active genes resulted in a permanent switching between the two selectable marker genes and consequently the exp

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36

Hikida, Masaki, Yasunori Nakayama, Yumi Yamashita, Yoshio Kumazawa, Shin-Ichi Nishikawa, and Hitoshi Ohmori. "Expression of Recombination Activating Genes in Germinal Center B Cells: Involvement of Interleukin 7 (IL-7) and the IL-7 Receptor." Journal of Experimental Medicine 188, no. 2 (1998): 365–72. http://dx.doi.org/10.1084/jem.188.2.365.

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Mouse germinal center (GC) B cells have been shown to undergo secondary V(D)J (V, variable; D, diversity; J, joining) recombination (receptor editing) mediated by the reexpressed products of recombination activating gene (RAG)-1 and RAG-2. We show here that interleukin (IL)-7 as well as IL-4 was effective in inducing functional RAG products in mouse IgD+ B cells activated via CD40 in vitro. Blocking of the IL-7 receptor (IL-7R) by injecting an anti– IL-7R monoclonal antibody resulted in a marked suppression of the reexpression of RAG-2 and subsequent V(D)J recombination in the draining lymph n

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37

Dunda, O., and D. Corcos. "Recombining sequence recombination in normal kappa-chain-expressing B cells." Journal of Immunology 159, no. 9 (1997): 4362–66. http://dx.doi.org/10.4049/jimmunol.159.9.4362.

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Abstract Recombining sequence (RS) recombination is a DNA rearrangement that deletes one or two C kappa alleles in a large proportion of lambda-expressing B cells. Since its discovery, this recombination has been suggested to play a role in activating lambda gene rearrangements. A model involving a positive signal generated by RS recombination seems to be excluded, but another model that is still under consideration proposes that RS recombination removes DNA sequences within the kappa locus that would interfere with lambda gene assembly. Using PCR assays, we have found that kappa-expressing ce

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38

Bories, JC, JM Cayuela, P. Loiseau, and F. Sigaux. "Expression of human recombination activating genes (RAG1 and RAG2) in neoplastic lymphoid cells: correlation with cell differentiation and antigen receptor expression." Blood 78, no. 8 (1991): 2053–61. http://dx.doi.org/10.1182/blood.v78.8.2053.2053.

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Abstract Regulation of V-(D)-J recombinations that occur in antigen receptor encoding genes remains poorly understood. Recently, two genes, RAG1 and RAG2, that are able to activate rearrangement of synthetic recombination substrates were cloned in mouse and a human gene homologous to RAG1 was described. To define the differentiation stages corresponding to RAG1 and RAG2 RNA expression, we have studied a large number of B- and T-lymphoid neoplasias. First, we show that a human gene homologous to the murine RAG2 is transcribed in humans. Moreover, using a polymerase chain reaction approach, we h

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Bories, JC, JM Cayuela, P. Loiseau, and F. Sigaux. "Expression of human recombination activating genes (RAG1 and RAG2) in neoplastic lymphoid cells: correlation with cell differentiation and antigen receptor expression." Blood 78, no. 8 (1991): 2053–61. http://dx.doi.org/10.1182/blood.v78.8.2053.bloodjournal7882053.

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Regulation of V-(D)-J recombinations that occur in antigen receptor encoding genes remains poorly understood. Recently, two genes, RAG1 and RAG2, that are able to activate rearrangement of synthetic recombination substrates were cloned in mouse and a human gene homologous to RAG1 was described. To define the differentiation stages corresponding to RAG1 and RAG2 RNA expression, we have studied a large number of B- and T-lymphoid neoplasias. First, we show that a human gene homologous to the murine RAG2 is transcribed in humans. Moreover, using a polymerase chain reaction approach, we have shown

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Zhang, X. L., Y. S. Lu, J. C. Jian, and Z. H. Wu. "Cloning and expression analysis of recombination activating genes (RAG1/2) in red snapper (Lutjanus sanguineus)." Fish & Shellfish Immunology 32, no. 4 (2012): 534–43. http://dx.doi.org/10.1016/j.fsi.2012.01.001.

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SHEARD, M., K. SUGAYA, M. FURUTA, S. TSUDA, and Y. TAKAHAMA. "Heterogeneous Expression of Recombination Activating Genes and Surface CD5 in CD3 low CD4 + CD8 + Thymocytes." Scandinavian Journal of Immunology 43, no. 6 (1996): 619–25. http://dx.doi.org/10.1046/j.1365-3083.1996.d01-263.x.

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Greenhalgh, P., C. E. Olesen, and L. A. Steiner. "Characterization and expression of recombination activating genes (RAG-1 and RAG-2) in Xenopus laevis." Journal of Immunology 151, no. 6 (1993): 3100–3110. http://dx.doi.org/10.4049/jimmunol.151.6.3100.

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Abstract The primary repertoire of B and T cells is established by V(D)J recombination. Two closely linked genes, RAG-1 and RAG-2, are essential for this process, and have been identified in mice, humans, and chickens. To study lymphocyte development in Xenopus laevis, we have characterized RAG-1 and RAG-2 in this species and examined their patterns of expression. Degenerate oligonucleotides, based on the known highly conserved RAG-1 sequences, were used to amplify, by the polymerase chain reaction, a segment of Xenopus RAG-1 from genomic DNA. A product of expected size was obtained and used t

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Bashkirov, Vladimir I., Jeff S. King, Elena V. Bashkirova, Jacqueline Schmuckli-Maurer, and Wolf-Dietrich Heyer. "DNA Repair Protein Rad55 Is a Terminal Substrate of the DNA Damage Checkpoints." Molecular and Cellular Biology 20, no. 12 (2000): 4393–404. http://dx.doi.org/10.1128/mcb.20.12.4393-4404.2000.

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ABSTRACT Checkpoints, which are integral to the cellular response to DNA damage, coordinate transient cell cycle arrest and the induced expression of DNA repair genes after genotoxic stress. DNA repair ensures cellular survival and genomic stability, utilizing a multipathway network. Here we report evidence that the two systems, DNA damage checkpoint control and DNA repair, are directly connected by demonstrating that the Rad55 double-strand break repair protein of the recombinational repair pathway is a terminal substrate of DNA damage and replication block checkpoints. Rad55p was specificall

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Papavasiliou, F. Nina, and David G. Schatz. "The Activation-induced Deaminase Functions in a Postcleavage Step of the Somatic Hypermutation Process." Journal of Experimental Medicine 195, no. 9 (2002): 1193–98. http://dx.doi.org/10.1084/jem.20011858.

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Activation of B cells by antigen fuels two distinct molecular modifications of immunoglobulin (Ig) genes. Class-switch recombination (CSR) replaces the Igμ heavy chain constant region with a downstream constant region gene, thereby altering the effector function of the resulting antibodies. Somatic hypermutation (SHM) introduces point mutations into the variable regions of Ig genes, thereby changing the affinity of antibody for antigen. Mechanistic overlap between the two reactions has been suggested by the finding that both require the activation-induced cytidine deaminase (AID). It has been

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Castro-Pérez, Edgardo, Emilio Soto-Soto, Marizabeth Pérez-Carambot, et al. "Identification and Characterization of the V(D)J Recombination Activating Gene 1 in Long-Term Memory of Context Fear Conditioning." Neural Plasticity 2016 (2016): 1–19. http://dx.doi.org/10.1155/2016/1752176.

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An increasing body of evidence suggests that mechanisms related to the introduction and repair of DNA double strand breaks (DSBs) may be associated with long-term memory (LTM) processes. Previous studies from our group suggested that factors known to function in DNA recombination/repair machineries, such as DNA ligases, polymerases, and DNA endonucleases, play a role in LTM. Here we report data using C57BL/6 mice showing that theV(D)J recombination-activating gene 1(RAG1), which encodes a factor that introduces DSBs in immunoglobulin and T-cell receptor genes, is induced in the amygdala, but n

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Liu, Yuchen, Nan Jiang, Wenzhi Liu, et al. "Rag1 and Rag2 Gene Expressions Identify Lymphopoietic Tissues in Larvae of Rice-Field Eel (Monopterus albus)." International Journal of Molecular Sciences 23, no. 14 (2022): 7546. http://dx.doi.org/10.3390/ijms23147546.

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In immature lymphocytes, recombination activating genes 1 and 2 are necessary for antigen receptor V (D) J recombination, representing immature lymphocyte biomarkers. Herein, we cloned and sequenced rice-field eel rag1 and rag2 genes. Their expressions in the thymus, liver, and kidney were significant from 0 days post hatching (dph) to 45 dph, peaking at 45 dph in these three tissues. In situ hybridization detected high rag1 and rag2 expressions in the liver, kidney, and thymus of rice-field eel from 2 to 45 dph, suggesting that multiple tissues of rice-field eel contain lymphocyte lineage cel

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Ji, Yanhong, Alicia J. Little, Joydeep K. Banerjee, et al. "Promoters, enhancers, and transcription target RAG1 binding during V(D)J recombination." Journal of Experimental Medicine 207, no. 13 (2010): 2809–16. http://dx.doi.org/10.1084/jem.20101136.

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V(D)J recombination assembles antigen receptor genes in a well-defined order during lymphocyte development. This sequential process has long been understood in the context of the accessibility model, which states that V(D)J recombination is regulated by controlling the ability of the recombination machinery to gain access to its chromosomal substrates. Indeed, many features of “open” chromatin correlate with V(D)J recombination, and promoters and enhancers have been strongly implicated in creating a recombinase-accessible configuration in neighboring chromatin. An important prediction of the a

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Meffre, Eric, Fotini Papavasiliou, Paul Cohen, et al. "Antigen Receptor Engagement Turns off the V(D)J Recombination Machinery in Human Tonsil B Cells." Journal of Experimental Medicine 188, no. 4 (1998): 765–72. http://dx.doi.org/10.1084/jem.188.4.765.

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The germinal center (GC) is an anatomic compartment found in peripheral lymphoid organs, wherein B cells undergo clonal expansion, somatic mutation, switch recombination, and reactivate immunoglobulin gene V(D)J recombination. As a result of somatic mutation, some GC B cells develop higher affinity antibodies, whereas others suffer mutations that decrease affinity, and still others may become self-reactive. It has been proposed that secondary V(D)J rearrangements in GCs might rescue B cells whose receptors are damaged by somatic mutations. Here we present evidence that mature human tonsil B ce

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Nicolas, Nathalie, Despina Moshous, Marina Cavazzana-Calvo, et al. "A Human Severe Combined Immunodeficiency (SCID) Condition with Increased Sensitivity to Ionizing Radiations and Impaired V(D)J Rearrangements Defines a New DNA Recombination/Repair Deficiency." Journal of Experimental Medicine 188, no. 4 (1998): 627–34. http://dx.doi.org/10.1084/jem.188.4.627.

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The products of recombination activating gene (RAG)1 and RAG2 initiate the lymphoid-specific phase of the V(D)J recombination by creating a DNA double-strand break (dsb), leaving hairpin-sealed coding ends. The next step uses the general DNA repair machinery of the cells to resolve this dsb. Several genes involved in both V(D)J recombination and DNA repair have been identified through the analysis of in vitro mutants (Chinese hamster ovary cells) and in vivo situations of murine and equine severe combined immunodeficiency (scid). These studies lead to the description of the Ku–DNA-dependent pr

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Smith, J., and R. Rothstein. "A mutation in the gene encoding the Saccharomyces cerevisiae single-stranded DNA-binding protein Rfa1 stimulates a RAD52-independent pathway for direct-repeat recombination." Molecular and Cellular Biology 15, no. 3 (1995): 1632–41. http://dx.doi.org/10.1128/mcb.15.3.1632.

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In the yeast Saccharomyces cerevisiae, recombination between direct repeats is synergistically reduced in rad1 rad52 double mutants, suggesting that the two genes define alternate recombination pathways. Using a classical genetic approach, we searched for suppressors of the recombination defect in the double mutant. One mutation that restores wild-type levels of recombination was isolated. Cloning by complementation and subsequent physical and genetic analysis revealed that it maps to RAF1. This locus encodes the large subunit of the single-stranded DNA-binding protein complex, RP-A, which is

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