Готові списки джерел за темами / V(D)J rearrangement

Добірка наукової літератури з теми "V(D)J rearrangement"

Автор: Grafiati
Опубліковано: 15 вересня 2021
Оновлено: 12 лютого 2022

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Статті в журналах з теми "V(D)J rearrangement":

1

Aster, J. C., and J. Sklar. "Interallelic V(D)J trans-rearrangement within the beta T cell receptor gene is infrequent and occurs preferentially during attempted D beta to J beta joining." Journal of Experimental Medicine 175, no. 6 (June 1, 1992): 1773–82. http://dx.doi.org/10.1084/jem.175.6.1773.

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Previous work has demonstrated that intergenic V(D)J rearrangement, a process referred to as trans-rearrangement, occurs at an unexpectedly high frequency. These rearrangements generate novel V(D)J combinations which could conceivably have some role in the normal immune system, and since they probably arise through chromosomal rearrangements akin to those associated with lymphoid neoplasia, they may also serve as a model for investigating recombinational events which underlie oncogenesis. In view of the existence of a mechanism that permits relatively frequent intergenic trans-rearrangements, it seems reasonable that interallelic trans-rearrangements involving segments belonging to each of the two alleles of a single antigen receptor gene might also occur. To determine the frequency of such rearrangements, we examined thymocytes of F1 progeny of a cross between SWR mice, which have a deletion spanning 10 of the known V beta segments, and NZW mice, which have a deletion involving all J beta 2 segments. Rearranged TCR-beta genes containing V beta segments from the NZW chromosome and J beta segments from the SWR chromosome were amplified from the DNA of F1 thymocytes with the polymerase chain reaction. Using this approach, we found that such rearrangements are relatively uncommon, being present in about 1 in 10(5) thymocytes, a frequency lower than that of V gamma/J beta intergenic trans-rearrangements. The ratio of conventional cis-rearrangement to interallelic trans-rearrangement for any particular V beta segment appears to be about 10(4):1. The structure of the junctions in all trans-rearrangements analyzed closely resembles conventional cis-rearrangements, indicating involvement of V(D)J recombinase in the ultimate joining event. However, in contrast to cis-rearrangements, a strong bias for inclusion of D beta 1 segments over D beta 2 segments was noted, suggesting that interallelic trans-rearrangement may occur preferentially during attempted D-J joining. J beta 2 segment usage in trans-rearrangements also appeared to differ from that expected from previously studied cis-rearrangements. The results have implications with respect to the events and timing of conventional cis-rearrangement during thymocyte differentiation, and the prevalence of various types of trans-rearrangements.
2

Hendrickson, E. A., V. F. Liu, and D. T. Weaver. "Strand breaks without DNA rearrangement in V (D)J recombination." Molecular and Cellular Biology 11, no. 6 (June 1991): 3155–62. http://dx.doi.org/10.1128/mcb.11.6.3155.

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Somatic gene rearrangement of immunoglobulin and T-cell receptor genes [V(D)J recombination] is mediated by pairs of specific DNA sequence motifs termed signal sequences. In experiments described here, retroviral vectors containing V(D)J rearrangement cassettes in which the signal sequences had been altered were introduced into wild-type and scid (severe combined immune deficiency) pre-B cells and used to define intermediates in the V(D)J recombination pathway. The scid mutation has previously been shown to deleteriously affect the V(D)J recombination process. Cassettes containing a point mutation in one of the two signal sequences inhibited rearrangement in wild-type cells. In contrast, scid cells continued to rearrange these cassettes with the characteristic scid deletional phenotype. Using these mutated templates, we identified junctional modifications at the wild-type signal sequences that had arisen from strand breaks which were not associated with overall V(D)J rearrangements. Neither cell type was able to rearrange constructs which contained only a single, nonmutated, signal sequence. In addition, scid and wild-type cell lines harboring cassettes with mutations in both signal sequences did not undergo rearrangement, suggesting that at least one functional signal sequence was required for all types of V(D)J recombination events. Analysis of these signal sequence mutations has provided insights into intermediates in the V(D)J rearrangement pathway in wild-type and scid pre-B cells.
3

Hendrickson, E. A., V. F. Liu, and D. T. Weaver. "Strand breaks without DNA rearrangement in V (D)J recombination." Molecular and Cellular Biology 11, no. 6 (June 1991): 3155–62. http://dx.doi.org/10.1128/mcb.11.6.3155-3162.1991.

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Somatic gene rearrangement of immunoglobulin and T-cell receptor genes [V(D)J recombination] is mediated by pairs of specific DNA sequence motifs termed signal sequences. In experiments described here, retroviral vectors containing V(D)J rearrangement cassettes in which the signal sequences had been altered were introduced into wild-type and scid (severe combined immune deficiency) pre-B cells and used to define intermediates in the V(D)J recombination pathway. The scid mutation has previously been shown to deleteriously affect the V(D)J recombination process. Cassettes containing a point mutation in one of the two signal sequences inhibited rearrangement in wild-type cells. In contrast, scid cells continued to rearrange these cassettes with the characteristic scid deletional phenotype. Using these mutated templates, we identified junctional modifications at the wild-type signal sequences that had arisen from strand breaks which were not associated with overall V(D)J rearrangements. Neither cell type was able to rearrange constructs which contained only a single, nonmutated, signal sequence. In addition, scid and wild-type cell lines harboring cassettes with mutations in both signal sequences did not undergo rearrangement, suggesting that at least one functional signal sequence was required for all types of V(D)J recombination events. Analysis of these signal sequence mutations has provided insights into intermediates in the V(D)J rearrangement pathway in wild-type and scid pre-B cells.
4

Lauzurica, P., and M. S. Krangel. "Temporal and lineage-specific control of T cell receptor alpha/delta gene rearrangement by T cell receptor alpha and delta enhancers." Journal of Experimental Medicine 179, no. 6 (June 1, 1994): 1913–21. http://dx.doi.org/10.1084/jem.179.6.1913.

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To analyze the regulation of gene rearrangement at the T cell receptor (TCR) alpha/delta locus during T cell development, we generated transgenic mice carrying a human TCR delta gene minilocus. We previously showed that the presence of the TCR delta enhancer (E delta) within the J delta 3-C delta intron was required to activate a specific step (V-D to J) of transgene rearrangement, and that rearrangement was activated equivalently in the precursors of alpha beta and gamma delta T cells. To further explore the role of transcriptional enhancers in establishing the developmental pattern of gene rearrangement at the TCR alpha/delta locus, we substituted the TCR alpha enhancer (E alpha) in place of E delta within the transgenic minilocus. We found that V-D-J rearrangement of the E alpha+ minilocus was restricted to the alpha beta T cell subset. Further, we found that although V-D-J rearrangement of the E delta+ minilocus was initiated in the fetal thymus by day 14.5, V-D-J rearrangement of the E alpha+ minilocus did not occur until fetal day 16.5. Finally, whereas V-D-J rearrangement of the E delta+ minilocus is essentially completed within the triple negative population of postnatal thymocytes, V-D-J rearrangement of the E alpha+ minilocus is only initiated late within this population. Since the properties of minilocus rearrangement under the control of E delta and E alpha parallel the properties of V delta-D delta-J delta and V alpha-J alpha rearrangement at the endogenous TCR alpha/delta locus, we conclude that these enhancers play an important role in orchestrating the developmental program of rearrangements at this locus.
5

Bain, Gretchen, William J. Romanow, Karen Albers, Wendy L. Havran, and Cornelis Murre. "Positive and Negative Regulation of V(D)J Recombination by the E2A Proteins." Journal of Experimental Medicine 189, no. 2 (January 18, 1999): 289–300. http://dx.doi.org/10.1084/jem.189.2.289.

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A key feature of B and T lymphocyte development is the generation of antigen receptors through the rearrangement and assembly of the germline variable (V), diversity (D), and joining (J) gene segments. However, the mechanisms responsible for regulating developmentally ordered gene rearrangements are largely unknown. Here we show that the E2A gene products are essential for the proper coordinated temporal regulation of V(D)J rearrangements within the T cell receptor (TCR) γ and δ loci. Specifically, we show that E2A is required during adult thymocyte development to inhibit rearrangements to the γ and δ V regions that normally recombine almost exclusively during fetal thymocyte development. The continued rearrangement of the fetal Vγ3 gene segment in E2A-deficient adult thymocytes correlates with increased levels of Vγ3 germline transcripts and increased levels of double-stranded DNA breaks at the recombination signal sequence bordering Vγ3. Additionally, rearrangements to a number of Vγ and Vδ gene segments used predominately during adult development are significantly reduced in E2A-deficient thymocytes. Interestingly, at distinct stages of T lineage development, both the increased and decreased rearrangement of particular Vδ gene segments is highly sensitive to the dosage of the E2A gene products, suggesting that the concentration of the E2A proteins is rate limiting for the recombination reaction involving these Vδ regions.
6

Dombret, H., P. Loiseau, JC Bories, and F. Sigaux. "Unexpected consistent involvement of V beta gene segments in inappropriate T-cell receptor beta gene rearrangements occurring in B- lineage acute lymphoblastic leukemias." Blood 80, no. 10 (November 15, 1992): 2614–21. http://dx.doi.org/10.1182/blood.v80.10.2614.2614.

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Abstract T-cell receptor beta (TCR beta) gene rearrangements occur in a third of early B-cell acute lymphoblastic leukemias (ALLs). V, D, and J segments involved in these inappropriate rearrangements remain unknown and are of interest, both because partial D beta J beta and complete V beta D beta J beta recombinations occur at distinct stages of thymic maturation and because these rearrangements are regulated differently. We have therefore studied in detail seven cases of B-lineage ALL that show inappropriate clonal TCR beta gene rearrangements. Analysis of genomic DNA by Southern hybridization with C beta, J beta 1, V beta 8, and V beta 11 probes suggested the involvement of V beta segment in tumor cell rearrangements. A complete genomic library constructed from one case was screened with a C beta probe, and the TCR beta gene rearrangement was cloned and fully sequenced to show an out of frame V beta 2.2-J beta 2.6 recombination. TCR beta gene rearrangements occurring in other cases were further analyzed by polymerase chain reaction (PCR) using J beta and V beta primers and the resulting specific PCR products were sequenced. Evidence of clonal V beta rearrangements was obtained in all cases. These unexpected findings represent the first definitive demonstration that complete V beta(D beta)J beta rearrangements can occur in B-lineage cells and contrast with the previously reported lack of V beta(D beta)J beta rearrangement in B cells from V beta-J beta-C beta-E mu transgenic mice. In the context of increasing evidence that rearrangements are linked to transcription of unrearranged gene segments, these data prompt a search in B-lineage ALL cells for the presence of germline V beta transcripts whose deregulated expression may be linked to early transforming events.
7

Dombret, H., P. Loiseau, JC Bories, and F. Sigaux. "Unexpected consistent involvement of V beta gene segments in inappropriate T-cell receptor beta gene rearrangements occurring in B- lineage acute lymphoblastic leukemias." Blood 80, no. 10 (November 15, 1992): 2614–21. http://dx.doi.org/10.1182/blood.v80.10.2614.bloodjournal80102614.

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T-cell receptor beta (TCR beta) gene rearrangements occur in a third of early B-cell acute lymphoblastic leukemias (ALLs). V, D, and J segments involved in these inappropriate rearrangements remain unknown and are of interest, both because partial D beta J beta and complete V beta D beta J beta recombinations occur at distinct stages of thymic maturation and because these rearrangements are regulated differently. We have therefore studied in detail seven cases of B-lineage ALL that show inappropriate clonal TCR beta gene rearrangements. Analysis of genomic DNA by Southern hybridization with C beta, J beta 1, V beta 8, and V beta 11 probes suggested the involvement of V beta segment in tumor cell rearrangements. A complete genomic library constructed from one case was screened with a C beta probe, and the TCR beta gene rearrangement was cloned and fully sequenced to show an out of frame V beta 2.2-J beta 2.6 recombination. TCR beta gene rearrangements occurring in other cases were further analyzed by polymerase chain reaction (PCR) using J beta and V beta primers and the resulting specific PCR products were sequenced. Evidence of clonal V beta rearrangements was obtained in all cases. These unexpected findings represent the first definitive demonstration that complete V beta(D beta)J beta rearrangements can occur in B-lineage cells and contrast with the previously reported lack of V beta(D beta)J beta rearrangement in B cells from V beta-J beta-C beta-E mu transgenic mice. In the context of increasing evidence that rearrangements are linked to transcription of unrearranged gene segments, these data prompt a search in B-lineage ALL cells for the presence of germline V beta transcripts whose deregulated expression may be linked to early transforming events.
8

Hendrickson, E. A., M. S. Schlissel, and D. T. Weaver. "Wild-type V(D)J recombination in scid pre-B cells." Molecular and Cellular Biology 10, no. 10 (October 1990): 5397–407. http://dx.doi.org/10.1128/mcb.10.10.5397.

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Homozygous mutation at the scid locus in the mouse results in the aberrant rearrangement of immunoglobulin and T-cell receptor gene segments. We introduced a retroviral vector containing an inversional immunoglobulin rearrangement cassette into scid pre-B cells. Most rearrangements were accompanied by large deletions, consistent with previously characterized effects of the scid mutation. However, two cell clones were identified which contained perfect reciprocal fragments and wild-type coding joints, documenting, on a molecular level, the ability of scid pre-B cells to generate functional protein-coding domains. Subsequent rearrangement of the DGR cassette in one of these clones was accompanied by a deletion, suggesting that this cell clone had not reverted the scid mutation. Indeed, induced rearrangement of the endogenous kappa loci in these two cell clones resulted in a mixture of scid and wild-type V-J kappa joints, as assayed by a polymerase chain reaction and DNA sequencing. In addition, three immunoglobulin mu- scid pre-B cell lines showed both scid and wild-type V-J kappa joins. These experiments strongly suggest that the V(D)J recombinase activity in scid lymphoid cells is diminished but not absent, consistent with the known leakiness of the scid mutation.
9

Hendrickson, E. A., M. S. Schlissel, and D. T. Weaver. "Wild-type V(D)J recombination in scid pre-B cells." Molecular and Cellular Biology 10, no. 10 (October 1990): 5397–407. http://dx.doi.org/10.1128/mcb.10.10.5397-5407.1990.

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Homozygous mutation at the scid locus in the mouse results in the aberrant rearrangement of immunoglobulin and T-cell receptor gene segments. We introduced a retroviral vector containing an inversional immunoglobulin rearrangement cassette into scid pre-B cells. Most rearrangements were accompanied by large deletions, consistent with previously characterized effects of the scid mutation. However, two cell clones were identified which contained perfect reciprocal fragments and wild-type coding joints, documenting, on a molecular level, the ability of scid pre-B cells to generate functional protein-coding domains. Subsequent rearrangement of the DGR cassette in one of these clones was accompanied by a deletion, suggesting that this cell clone had not reverted the scid mutation. Indeed, induced rearrangement of the endogenous kappa loci in these two cell clones resulted in a mixture of scid and wild-type V-J kappa joints, as assayed by a polymerase chain reaction and DNA sequencing. In addition, three immunoglobulin mu- scid pre-B cell lines showed both scid and wild-type V-J kappa joins. These experiments strongly suggest that the V(D)J recombinase activity in scid lymphoid cells is diminished but not absent, consistent with the known leakiness of the scid mutation.
10

Agard, Emily A., and Susanna M. Lewis. "Postcleavage Sequence Specificity in V(D)J Recombination." Molecular and Cellular Biology 20, no. 14 (July 15, 2000): 5032–40. http://dx.doi.org/10.1128/mcb.20.14.5032-5040.2000.

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ABSTRACT Unintended DNA rearrangements in a differentiating lymphocyte can have severe, oncogenic consequences, but the mechanisms for avoiding pathogenic outcomes in V(D)J recombination are not well understood. The first level at which fidelity is instituted is in discrimination by the recombination proteins between authentic and inauthentic recombination signal sequences. Nevertheless, this discrimination is not absolute and cannot fully eliminate targeting errors. To learn more about the basis of specificity during V(D)J recombination, we have investigated whether it is possible for the recombination machinery to detect an inaccurately targeted sequence subsequent to cleavage. These studies indicate that even postcleavage steps in V(D)J recombination are sequence specific and that noncanonical sequences will not efficiently support the resolution of recombination intermediates in vivo. Accordingly, interventions after a mistargeting event conceivably occur at a late stage in the joining process and the likelihood may well be crucial to enforcing fidelity during antigen receptor gene rearrangement.
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Статті в журналах Дисертації Книги

Дисертації з теми "V(D)J rearrangement":

1

Cieslak, Agata. "Normal and pathological mechanisms of TCRα/δ locus rearrangement in thymic lymphopoiesis". Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB112.

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La maturation des cellules lymphoïdes T est un processus thymique hautement régulé au cours duquel les réarrangements ordonnés des loci du TCRδ, y, β et enfin α déterminent le développement des lignées yδ et αβ. Les remaniements somatiques des segments géniques V, (D) et J du TCR font intervenir les protéines RAG1/2, les séquences RSS jouxtant ces segments et des éléments régulateurs (enhancers) assurant une cis-régulation de ce processus. Le contrôle de la recombinaison V(D)J se fait grâce à divers mécanismes incluant des mécanismes épigénétiques, l’intervention de facteurs de transcription et la conformation/séquence des RSS. Dans ce travail, nous montrons que les réarrangements du locus TCRδ sont strictement ordonnés chez l’Homme. Le premier réarrangement Dδ2-Dδ3 se produit à un stade ETP (Early T-cell Precursor) CD34+/CD1a-/CD7+dim, et précède systématiquement le réarrangement Dδ2-Jδ1. L’analyse in silico du locus a permis d’identifier un site de fixation clé pour le facteur de transcription RUNX1 à proximité immédiate de l’heptamètre Dδ2-23RSS chez l’Homme mais absent chez la souris. Le recrutement de RUNX1 sur ce site dans les thymocytes très immatures CD34+/CD3- permet d’augmenter l’affinité de fixation des protéines RAG1/2 sur le Dδ2-23RSS de manière spécifique. Ce travail identifie un rôle original de cofacteur de RUNX1 au cours de la recombinaison V(D)J dans la thymopoïèse humaine. Une série d’analyses épigénétiques exhaustives, menées dans le cadre du projet Européen Blueprint, sur les sous-populations thymiques humaines, nous a permis d’établir que l’enhanceosome du TCRα est constitué, comme chez la souris, dès les étapes les plus précoces de la thymopoïèse sans pour autant pouvoir s’activer avant la fin de la β-sélection. Nos résultats préliminaires suggèrent que les protéines homéotiques HOXA (notamment HOXA9) répriment l’activité de l’enhancer alpha (et donc les réarrangements du TCRα en interagissant avec le facteur de transcription ETS1 via leurs homéodomaines. Leur répression, induite par le passage de la β-sélection, aboutit à l’ouverture chromatinienne des segments Vα/Jα via l’activation du TCRα. Ces résultats apportent un éclairage nouveau sur le découplage jusqu’ici inexpliqué entre la formation de l’enhanceosome du TCRα à un stade très immature et son activation, permettant les réarrangements du locus, à un stade thymique bien plus tardif
Maturation of T lymphoid cells is a highly regulated process where ordered thymic rearrangements at the TCRδ, TCRy, TCRβ and finally TCRα loci determine the development into either yδ or αβ T-cell lineages. Somatic rearrangements of V, (D), and J gene segments of TCR loci involve RAG1/2 proteins, RSS sequences juxtaposing V, D, and J genes segments and regulatory elements (enhancers) providing a cis-regulation of this process. The control of the V(D)J recombination is achieved through various mechanisms including epigenetic modifications, involvement of transcription factors and RSS conformation/sequence. In this work, we show that TCRδ rearrangements are strictly ordered in Humans. The first Dδ2-Dδ3 rearrangement occurs at ETP (Early T-Cell Precursor) stage CD34+/CD1a-/CD7+dim, and always precedes Dδ2-Jδ1 rearrangement. In-silico analysis of the locus identified a key binding site for a transcription factor RUNX1 in close proximity to the Dδ2-23RSS heptamer in human, but not in mice. The RUNX1 recruitment at this site in immature CD34+/CD3- thymocytes increases binding affinity of RAG1/2 proteins. This work identifies an original cofactor of human VDJ recombination. A set of comprehensive epigenetic analysis conducted within the Europeen Blueprint project on human thymic subpopulations allowed as to establish that the TCRα enhanceosome (Eα), as in mice, is already formed from the earliest stages of thymopoiesis without being able to be activated before the end of β-selection. Our preliminary results suggest that HOXA homeobox proteins (including HOXA9) suppress the activity of the Eα (thus TCRα rearrangements) by interacting with the transcription factor ETS1 via their homeodomains. Induced by β-selection HOXA repression results in the chromatin opening of the Vα/Jα gene segments through TCRα activation. These finding shed new light on the so far unexplained shift observed between the formation of Eα enhanceosome at a very immature stages and its activation at a much later developmental stages
2

Vesprini, Danny. "Illegitimate V(D)J rearrangement in ã-irradiation induced T cell lymphoma in newborn scid mice." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq29263.pdf.

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3

Li, Shuang. "Molecular mechanisms leading to the emergence of mouse regulatory T lymphocytes specific to non-inherited maternal antigens." Doctoral thesis, Universite Libre de Bruxelles, 2021. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/327043.

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[EN]It is well illustrated that the generation of Tregs is the main mechanism responsible for maintaining immune tolerance during developmental exposure to non-inherited maternal antigen (NIMA). Moreover, the presence of NIMA-specific Tregs in the uterus of pregnant mice promote reproductive fitness by enforcing maternal tolerance to overlapping paternal antigens expressed by the fetus during next-generation pregnancies. However, the reason why perinatal T cell lineage is biased towards immune tolerance is poorly understood. Due to the fact that terminal deoxynucleotidyl transferase (TdT) is not expressed in neonatal T cells in the mouse, neonatal T cells have a less diverse TCR repertoire. This is known to limit their specificity and to increase their affinity for MHC/peptide complexes. At the start of the present work, we postulated that expressing high affinity TCR might be the reason that forces the development of antigen-specific Tregs in neonates. We undertook our study with the aim to investigate the mechanisms underlying mouse NIMA-specific Treg development in the perinatal period. Using 2W1S-OVA+ heterozygous mouse model in which 2W1S antigen was transformed into surrogate NIMA for half of the offspring, we observed an increased frequency of 2W1S-specific Tregs in NIMA-2W1S-exposed animals. Moreover, we also observed that periphery-derived NIMA-2W1S Tregs had a less diverse TCR repertoire and were phenotypically distinct from thymus-derived SELF-2W1S-specific Tregs. In order to investigate whether the lack of diversity was responsible for the development of neonatal NIMA-specific Tregs, we generated transgenic mice where TdT expression was enforced in T cells before birth. We found that transgenic TdT added clonal TCR diversity but did not prevent the development of T cell clones with neonatal type TCR repertoire and did not modify the frequency of neonatal NIMA-specific Tregs. On the contrary, TdT expression increased significantly generation of SELF-specific Tregs to levels similar to that of NIMA-specific Tregs. Taken together, our data indicate that the developmental pathways of NIMA- and SELF-specific Treg repertoire are different in terms of inducing and maintaining neonatal tolerance.
[FR]Il est bien illustré que la génération périnatal de Treg est le principal mécanisme responsable du maintien de la tolérance immunitaire fœtale qui se développe suite à l'exposition aux antigènes maternels non-hérités (NIMA). De plus, la présence de Tregs spécifiques des NIMA dans l'utérus des femmes enceintes favorise la capacité de reproduction en renforçant la tolérance maternelle aux mêmes antigènes paternels exprimés par le fœtus pendant les grossesses de prochaine génération. Cependant, la raison pour laquelle la lignée des cellules T fœtales est biaisée en faveur de la tolérance immunitaire est mal comprise. Chez la souris, en raison du manque d'expression de la désoxynucléotidyl transférase terminale (TdT), les cellules T néonatales ont un répertoire de TCR moins diversifié. Ceci est connu pour limiter leur spécificité et augmenter leur affinité pour les complexes CMH / peptide. Au début du présent travail, nous avons émis l'hypothèse que l'expression de TCRs de haute affinité pourrait être la raison qui force le développement de Treg spécifiques chez les nouveau-nés. Nous avons plus particulièrement entrepris notre étude dans le but d'étudier les mécanismes sous-jacents au développement de Tregs spécifiques des NIMA chez la souris pendant la période périnatale. En utilisant le modèle de souris hétérozygotes pour 2W1S-OVA+ dans lequel l'antigène 2W1S a été transformé en NIMA pour la moitié de la progéniture, nous avons observé une fréquence accrue de Tregs spécifiques de 2W1S chez les animaux exposés au NIMA. De plus, nous avons également observé que les Treg NIMA-2W1S dérivés de la périphérie avaient un répertoire de TCRs moins diversifié et étaient phénotypiquement distincts des Tregs spécifiques de SELF-2W1S dérivés du thymus. Afin de déterminer si le manque de diversité était responsable du développement de Tregs néonataux spécifiques de NIMA, nous avons généré des souris transgéniques où l'expression de TdT était appliquée dans les cellules T avant la naissance. Nous avons constaté que le TdT transgénique ajoutait une diversité de TCR clonale, mais n'empêchait pas le développement de clones de cellules T avec un répertoire TCR de type néonatal et ne modifiait pas la fréquence des Treg néonataux spécifiques du NIMA. Au contraire, l'expression de TdT a augmenté de manière significative la génération de Tregs spécifiques de SELF-2W1S à des niveaux similaires à ceux des Treg spécifiques de NIMA-2W1S. Prises ensembles, nos données indiquent que les voies de développement du répertoire des Tregs néonataux spécifiques de NIMA et SELF sont différentes en termes d'induction et de maintien de la tolérance néonatale.
Doctorat en Sciences biomédicales et pharmaceutiques (Médecine)
info:eu-repo/semantics/nonPublished
4

Wagatsuma, Keisuke. "STAT5 Orchestrates Local Epigenetic Changes for Chromatin Accessibility and Rearrangements by Direct Binding to the TCRγ Locus". 京都大学 (Kyoto University), 2016. http://hdl.handle.net/2433/204582.

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5

Bianchi, Joy J. "Origin of somatic mutations in lymphoid cancers : role of the V(D)J recombinase Breakage-fusion-bridge events trigger complex genome rearrangements and amplifications in developmentally arrested T cell lymphomas End donation errors at antigen receptor loci trigger genome-wide instability in ATM-deficient T cell lymphomas." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB057.

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Les cancers lymphoïdes présentent fréquemment des aberrations chromosomiques. Dans les lymphocytes, cette instabilité génomique peut découler d'une activité anormale de la recombinase V(D)J (i.e. RAG endonuclease), alors que des facteurs de réponse aux dommages à l'ADN (DDR), tels que les protéines Ataxia-telangiectasia mutated (ATM) et p53, sont connus pour empêcher l'apparition de réarrangements chromosomiques et la lymphomagénèse. Le but de ma thèse fut de tester la contribution relative de ces facteurs dans l'émergence des mutations somatiques dans le génome des lymphomes. Pour ce faire, j'ai réalisé du séquençage génome et transcriptome entier de différents lymphomes, issus de modèles murins génétiquement modifiés pour lesquels les activités RAG et DDR étaient altérées. Lors d'une première étude, j'ai identifié des lésions génomiques spécifiques et récurrentes, causées par l'activité « off-target » de RAG et, de manière plus surprenante, un pattern de réarrangements anormaux survenant en l'absence de RAG. J'ai mis en évidence un mécanisme de « Breakage-Fusion-Bridge », en l'absence de RAG, entrainant l'instabilité et l'amplification d'une région génomique s'étendant sur plusieurs mégabases. Plus encore, j'ai également montré que cette amplification mène à son tour à la surexpression de multiples gènes connus ou candidats dans le cancer et se retrouve dans un sous-groupe de leucémies humaines. Afin de rétablir la différentiation des cellules T, bloquée en l'absence des RAG, j'ai utilisé un autre modèle murin exprimant un récepteur des cellules T (TCR) transgéniques. Ce travail a permis de montrer que le stade du développement et l'activité RAG tous les deux déterminent le paysage génomique des lymphomes T et guident la transformation maligne des cellules à travers différentes voies oncogéniques. De plus, j'ai également réalisé la première étude génome entier de lymphomes T déficients pour ATM et ai identifié un nombre important d'anomalies dans ces tumeurs, présentes aux loci des récepteurs aux antigènes mais aussi à des positions ectopiques. Mes résultats suggèrent, qu'en l'absence d'ATM, les cassures de l'ADN induites par les RAG (non réparées ou résolues de manière anormales) déclenchent une instabilité massive au niveau des loci des récepteurs aux antigènes. Cette instabilité se propage ensuite ailleurs dans le génome et affecte des gènes du cancer. De manière plus générale, ma thèse approfondie la compréhension des mécanismes générant des mutations somatiques dans les cancers lymphoïdes, suite à des défauts de recombinaison V(D)J ou de DDR
Lymphoid cancers frequently harbor chromosomal aberrations. Abnormal V(D)J recombinase (i.e RAG endonuclease) activity is thought to promote genomic instability in lymphocytes, while DNA damage response (DDR) factors such as Ataxia-telangiectasia mutated (ATM) and p53 have been shown to suppress aberrant chromosomal rearrangements and lymphomagenesis. During my thesis, to test the relative contribution of these factors in shaping the pattern of somatic mutations in lymphoma genome, I performed whole genome and transcriptome sequencing of several genetically modified mouse lymphoma models in which the activities of RAG and DDR were perturbed. In a first study, I have identified specific recurrent genomic lesions caused by off-target RAG activity and, more surprisingly, a unique pattern of aberrant rearrangements occurring in the absence of RAG. I provided evidence that, in the absence of RAG, Breakage-Fusion-Bridge triggers instability and amplification of a genomic region of several megabases leading to the overexpression of multiple known and putative cancer genes. Importantly, I also showed that this region is found amplified in a subset of human leukemia. Using additional animal models in which blocked T cell differentiation due to the absence of RAG was rescued by the expression of a transgenic T cell receptor, I could demonstrate that both developmental stage and RAG activity determine T cell lymphoma genome landscapes and mediate malignant transformation through distinct oncogenic paths. In addition, I have established the first genome-wide analysis of ATM-deficient T-cell lymphomas and identified a high number of aberrations localized at antigen receptor loci and ectopic locations in these tumors. My results suggest that, in the absence of ATM, aberrantly resolved RAG-induced DNA breaks at antigen receptor loci trigger massive complex rearrangements spreading to ectopic locations and affecting cancer genes. Overall, my studies provide new insights into the mechanisms of somatic mutations arising in lymphoid cancers in the context of aberrant V(D)J recombination and DDR
6

COCEA, LAURENTIU. "Recherche et etude des elements regulateurs de rearrangement dans la region v-j du locus de la chaine legere d'immunoglobuline." Paris 5, 1999. http://www.theses.fr/1999PA05N037.

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7

Chovanec, Peter. "Studies of B cell development and V(D)J recombination." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/288271.

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The process of generating the vast diversity of immunoglobulin receptors and secreted antibodies begins with the recombination of the joining (JH), diversity (DH) and variable (VH) genes in the immunoglobulin heavy chain locus. The ability to produce antibodies is restricted to the B cell lineage and is tightly regulated, starting with the temporal separation of the recombination process, in which DH-JH precedes VH-DHJH recombination. Successful recombination of both heavy and light chain loci results in the expression of an antigen receptor on the cell surface. Subsequent selection stages remove non‑functional and autoreactivity receptors from the final pool of antigen responding B cells that ultimately give rise to antibody secreting plasma cells. Understanding the complexity of the recombination processes and the diversity of the resulting antibody repertoire has been a major focus of academic and industrial research alike. Therapeutic monoclonal antibodies have seen many successful applications within the clinic and they constitute a billion-dollar industry. However, limitations therein have resulted in the emergence of antibody engineering approaches and the use of natural sources of alternative heavy chain only antibodies (HCAbs/nanobodies). The biotechnology company Crescendo Biologics has taken the highly desired characteristics of HCAbs a step further with the creation of a mouse platform capable of producing fully humanized HCAbs. The Crescendo platform presents a unique opportunity to expand our understanding of how mouse B cell development functions by exploiting the features of heavy chain only antibody production. Furthermore, the platform enables the expansion of our limited knowledge of the epigenetic mechanisms involved in the recombination of the human immunoglobulin heavy chain locus. Using flow cytometry, with dimensionality reduction analysis approaches, I investigated B cell development in the context of HCAbs. These studies revealed a previously uncharacterised developmentally intermediate B cell population. Due to ethical and availability limitations to studies of human bone marrow, the primary pre-selection human B cell repertoire has not been studied in detail. The isolation of several B cell developmental stages and the use of our novel DNA-based high-throughput unbiased repertoire quantification technique, VDJ-seq, allowed me to study recombination of the human IGH locus sequence and observe HCAb repertoire selection within the mouse environment. The adaptation of next generation sequencing techniques to antigen receptor repertoire quantification has provided an unprecedented insight into repertoire diversity and the alterations it undergoes during infection or ageing. Our VDJ-seq assay is unique in its ability to interrogate DNA recombinants. To expand its capabilities, I investigated several limitations of the technique, including mispriming and PCR/sequencing errors, and implemented experimental and bioinformatics solutions to overcome them, which included the creation of a comprehensive analysis workflow. Finally, I have developed and applied a novel network visualisation method for genome-wide promoter interaction data generated by promoter capture Hi-C. The availability of high quality human pluripotent stem cell datasets allowed me to utilise the new techniques to further our understanding of the dynamics of genome organisation during early human embryonic development. This visualisation approach will be directly applicable to understanding B cell development.
8

Riedel, Frank [Verfasser], Fritz-V. [Gutachter] Kohl, H. J. [Gutachter] Peter, and J. [Gutachter] Witte. "Prävalenz schlafbezogener Atmungsstörungen bei Herzschrittmacherpatienten / Frank Riedel ; Gutachter: Fritz-V. Kohl, H. J. Peter, J. Witte." Berlin : Humboldt-Universität zu Berlin, 1998. http://d-nb.info/1207641383/34.

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9

Montpellier, Bertrand. "Recombinaison V(D)J illégitime et développement de leucémies aigues lymphoblastiques T." Aix-Marseille 2, 2008. http://theses.univ-amu.fr.lama.univ-amu.fr/2008AIX22086.pdf.

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La LAL-T est une hémopathie maligne qui représente 10-15% des LAL pédiatriques et 25% des LAL adultes. De manière alarmante, son incidence ne cesse de s’accroitre et son pronostic reste péjoratif malgré les améliorations de la prise en charge thérapeutique. L’amélioration du taux de survie des patients passe notamment par une compréhension accrue des mécanismes de pathogenèse. Dans ce contexte, le travail de thèse a été: 1) Partant de l’observation que de rares SJ chromosomiques réarrangent en cis par recombinaison V(D)J, nous avons émis l’hypothèse que les SJ épisomiques (ESJ) sont également réactifs en trans et peuvent ainsi réintégrer le génome. Nous montrons que d’un point de vue mécanistique les ESJ réarrangent efficacement en trans et que des cRSS présents à proximité d’oncogènes et ciblés dans la LAL-T lors de translocations chromosomiques constituent de bonnes cibles de réintégration. Nous démontrons de plus l’existence d’évènements de réintégration in vivo et estimons leur fréquence à ~1/104-6. La réintégration des ESJ constitue donc un évènement potentiel de dérégulation oncogénique. 2) Les évènements de recombinaison V(D)J légitimes ou illégitimes (translocations) sont hiérarchisés au cours du développement lymphocytaire. En tirant parti de notre connaissance des mécanismes de translocations chromosomiques, nous avons déterminé la cinétique d’acquisition d’une partie des activations oncogéniques présentes chez un patient LAL-T. De plus, l’identification chez ce patient d’un total de 10 évènements oncogéniques illustre le caractère multihit de cette maladie. La nature de ces évènements suggère un rôle potentiel de cMyc dans le caractère agressif de la LAL-T chez ce patient
T-ALL is a lymphoid neoplasia that accounts for 10-15% of pediatric ALL and 25% of adult ALL. Alarmingly, and despite indisputable success achieved in treatments its incidence is increasing and its prognostic remains pejorative. Survival rate outcome depend notably on a better understanding in pathogenic mechanisms. In this context, the thesis work has been the following: 1) Based on the observation that rare chromosomal SJ keep on recombining in cis using V(D)J recombination, we hypothesized that episomal SJ (ESJ) still remain reactives and can undergo genomic reintegration. We show that mechanistically, ESJ efficiently rearrange in trans and that the cRSS, the sequences targeted in oncogenic chromosomal translocations, are good ESJ integration sites. Moreover, we demonstrate the presence of ESJ reintegration events in vivo and estimate their frequency to ~1/104-6. In conclusion, ESJ reintegration is a potential mechanism of oncogenic deregulation. 2) Conventional and illegitimate V(D)J recombination events (e. G. Translocations) are ordered during lymphocyte development. Based on our knowledge on chromosomal translocation mechanisms, we determine the kinetics of a subset of oncogenic activations acquired during the transformation process in a T-ALL patient’s leukemic cells. Moreover, we identified up to 10 independent oncogenic events in this patient, illustrating the multi-hit characteristic of T-ALL. Finally, the oncogenic event’s functional impact suggests that cMyc play an important role in the particularly aggressive features of the T-ALL developed by this patient
10

Simonet, Maria-Ana. "Modélisation des réarrangements V(D)J au niveau du locus TRA/TRD." Université Joseph Fourier (Grenoble), 2008. http://www.theses.fr/2008GRE10302.

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Les lymphocytes T expriment à leur surface des récepteurs (TCR) composés de chaînes a~ ou y8, chargés de reconnaitre des peptides antigéniques. Une chaîne d'un TCRa donnée est le résultat de l'assemblage de gènes variable (V), jonction (J) et constant (C) sous le contrôle d'un mécanisme de recombinaison spécifique dénommé «recombinaison V(D)J ». De part le nombre important de gènes V et J dispersés sur plus de 1méga base et des segments V dupliqués chez la souris, il est quasiment impossible d'établir la diversité combinatoire VJ exacte et surtout leurs fréquences par les techniques actuelles de biologie moléculaire. Aussi pour appréhender ces questions, nous avons développé un modèle de simulation des ré arrangements des combinaisons VJ codant pour la chaine TCRa chez la souris. Le modèle implémenté est basé sur des fenêtres d'accessibilités flexibles, des vitesses d'ouverture variables et inclue aussi un temps de maturation entre deux ré arrangements. Il permet de rendre compte de la dynamique et de la variabilité de la chaine a en termes de répertoire (nombre et fréquence des combinaisons). Il propose que 2 à 3 réarrangements sont suffisant pour utiliser l'ensemble des segments J et permet aussi de donner un profil global de l'ensemble des combinaisons VJ. En parallèle, une analyse des réarrangements VJ a été réalisée chez l'homme. Cetteanalyse permet de visualiser les profils des combinaisons VJ expérimentaux et permettra de valider l'adaptation du modèle de simulation des réarrangements des chaines TCRa chez la souris aux chaines TCRa chez l'homme. Le modèle pourra servir d'outils pour analyser les variations entre répertoire sain et répertoire altéré ou modifié dans le cas de pathologies
T lymphocytes express at their surface an antigen receptor composed by a~ or y8 chains. A TCRa chains are encoded by a variable (V), ajoining (J) and a constant (C) segments which are under the of the control of a specific recombination mechanism called "V(D)J recombination". The VJ combinatorial diversity is unknown and the current state of molecular technology does not allow us to perform an analysis of aIl putative VJ combination or to estimate the frequencies of the functional VJ in mice. To overcome this difficulty we defined a mathematical model fitting experimental data. This model gives new insights on the mIes controlling the use of the V and the J genes and provides a dynamic ca1culation of the VJ combinations. The model proposes an accessibility of the TRAlTRD locus by sûccessive windows of different sizes and with different speed of progression. Furthermore, a possibility of successive secondary rearrangements was introduced. Ln parallel, an experimental analysis of the VJ combination has been performed in humans. From this analysis, the VJ combination profiles are ca1culated and used to validate our simulation program. Ln the future, the model may be use to analysis the variations between sound or altered repertoire
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Книги з теми "V(D)J rearrangement":

1

Vesprini, Danny. Illegitimate V(D)J rearrangement in gcs-irradiation induced T cell lymphoma in newborn scid mice. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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2

Ferrier, Pierre, ed. V(D)J Recombination. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0296-2.

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3

Sollbach, Astrid Elisabeth. Inversions produced during V(D)J recombination at IgH, the immunoglobulin heavy chain locus. Ottawa: National Library of Canada, 1994.

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4

Capasso, Mario. Come tele di ragno sgualcite: D.-V. Denon e J.-F. Champollion nell'Officina dei papiri ercolanesi. Napoli: Eurocomp 2000, 2002.

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5

Webber, Travis David. Characterization of Ig loci and V(D)J recombination activity in a population of Abelson murine leukemia virus-transformed pre-B cells derived from embryonic stem cells in vitro. Ottawa: National Library of Canada, 2002.

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6

Rights, European Court of Human. Affaires/Cases of A-Macaluso, B-Manunza, c-Gilberti, D-Nonnis, E-Trotto, F-Cattivera, G-Seri, H-Gori, I-Casadio, J-Testa, K-Covitti, L-Zonetti, M-Simonetti, N-Dal Sasso: Italie/v. Italy : arrêts du 3 Décembre 1991/judgments of 3 December 1991. Strasbourg: Greffe de la Cour, Conseil de l'Europe, 1992.

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7

United States. Congress. Senate. Committee on Armed Services. Nominations before the Senate Armed Services Committee, first session, 113th Congress: Hearings before the Committee on Armed Services, United States Senate, One Hundred Thirteenth Congress, first session, on nominations of Hon. Charles T. Hagel; Gen. Lloyd J. Austin III, USA; Gen. David M. Rodriguez, USA; Hon. Alan F. Estevez; Mr. Frederick E. Vollrath; Mr. Eric K. Fanning; Gen. Philip M. Breedlove, USAF; Gen. Martin E. Dempsey, USA; Adm James A Winnefeld, Jr., USN; Hon. Stephen W. Preston; Hon. Jon T. Rymer; Ms. Susan J. Rabern; Mr. Dennis V. McGinn; Adm Cecil E.D. Haney, USN; LTG Curtis M. Scaparrotti, USA; Hon. Deborah Lee James; Hon. Jessica Garfola Wright; Mr. Frank G. Klotz; Mr. Marcel J. Lettre II; Mr. Kevin A. Ohlson; Mr. Michael D. Lumpkin; Hon. Jamie M. Morin; and Hon. Jo Ann Rooney; January 31; February 12, 14, 28; April 11; July 18, 25, 30; September 19; October 10, 2013. Washington: U.S. Government Printing Office, 2014.

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8

Ramsden, Dale Andrew. Recombination and repertoire: the molecular biology of V(D)J rearrangement, and how V(D)J rearrangement affects B cell development and the B cell repertoire. 1993.

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9

1951-, Ferrier Pierre, ed. V(D)J recombination. New York, N.Y: Springer Science+Business Media, 2009.

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10

Murre, Cornelis. Long Range Regulation of V(d)J Recombination. Elsevier Science & Technology Books, 2015.

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Частини книг з теми "V(D)J rearrangement":

1

Swanson, Patrick C., Sushil Kumar, and Prafulla Raval. "Early Steps of V(D)J Rearrangement: Insights from Biochemical Studies of RAG-RSS Complexes." In Advances in Experimental Medicine and Biology, 1–15. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0296-2_1.

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2

Parks, Adam R., and Joseph E. Peters. "V(D)J Recombination." In Molecular Life Sciences, 1243–45. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-1531-2_170.

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3

Müschen, Markus. "V(D)J Recombination." In Encyclopedia of Cancer, 4773–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_6171.

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4

Müschen, Markus. "V(D)J Recombination." In Encyclopedia of Cancer, 3875–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_6171.

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5

Parks, Adam R., and Joseph E. Peters. "V(D)J Recombination." In Molecular Life Sciences, 1–4. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-6436-5_170-1.

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6

Müschen, Markus. "V(D)J Recombination." In Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-27841-9_6171-2.

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7

de Villartay, Jean-Pierre. "V(D)J Recombination Deficiencies." In Advances in Experimental Medicine and Biology, 46–58. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0296-2_4.

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8

Gellert, Martin. "V(D)J recombination: mechanism and consequences." In Molecular Genetics of Recombination, 469–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71021-9_16.

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9

Taccioli, G. E., G. Rathbun, Y. Shinkai, E. M. Oltz, H. Cheng, G. Whitmore, T. Stamato, P. Jeggo, and F. W. Alt. "Activities Involved in V(D)J Recombination." In Current Topics in Microbiology and Immunology, 107–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77633-5_13.

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10

Hsu, Ellen. "V(D)J Recombination: Of Mice and Sharks." In Advances in Experimental Medicine and Biology, 166–79. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0296-2_14.

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Тези доповідей конференцій з теми "V(D)J rearrangement":

1

Ru, Heng, Melissa G. Chambers, Maofu Liao, and Hao Wu. "Abstract B073: Structural basis of the 12-23 rule in V(D)J recombination." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b073.

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2

"A Novel Pipeline for V(D)J Junction Identification using RNA-Seq Paired-end Reads." In International Conference on Bioinformatics Models, Methods and Algorithms. SciTePress - Science and and Technology Publications, 2013. http://dx.doi.org/10.5220/0004247601850189.

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3

Ru, Heng, Melissa G. Chambers, Tian-Min Fu, Alexander B. Tong, Maofu Liao, and Hao Wu. "Abstract B122: Molecular mechanism of V(D)J recombination from synaptic RAG1-RAG2 complex structures." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-b122.

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4

Lee, Cheng-Sheng, Jiazhi Hu, and Frederick W. Alt. "Abstract B171: Elucidating the mechanism of RAG tracking and its impacts on V(D)J recombination." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-b171.

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5

Ba, Zhaoqing, Jiazhi Hu, Zhou Du, Sherry G. Lin, Duane R. Wesemann, and Frederick W. Alt. "Abstract A033: Mechanisms that mediate intralocus and interlocus regulation of V(D)J recombination at immunoglobulin light chain loci." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a033.

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6

Ba, Zhaoqing, Suvi Jain, Jiazhi Hu, and Frederick Alt. "Abstract B099: Elucidating the mechanisms that underpin RAG chromatin scanning in V(D)J recombination at antigen receptor gene loci." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-b099.

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7

Panta Pazos, Rube´n. "Finding the Minimun of the Quadratic Functional in Variational Approach in Transport Theory Problems." In 16th International Conference on Nuclear Engineering. ASMEDC, 2008. http://dx.doi.org/10.1115/icone16-48479.

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In this work it is reviewed the variational approach for some Transport Problems. Let X be a convex domain in Rn, and V a compact set. For that, it is considered the following equation: ∂ψ∂t(x,v,t)+v·∇ψ(x,v,t)+h(x,μ)ψ(x,v,t)==∫Vk(x,v,v′)ψ(x,v′,t)dv′+q(x,v,t)(1) where x represents the spatial variable in a domain D, v an element of a compact set V, Ψ is the angular flux, h(x,v) the collision frequency, k(x,v,v’) the scattering kernel function and q(x,v) the source function. It is put the attention in the construction of the quadratic functional J which appears in variational approaches for transport theory (for example, the Vladimirov functional). Some properties of this functional in a proper functional framework, in order to determine the minimum for J are considered. First, the general formulation is studied. Then an algorithm is given for minimizing the functional J for two remarkable problems: spherical harmonic method and spectral collocation method. A program associated to this algorithm is worked in a computer algebraic system, and also was depeloped a version in a high level language.
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Wang, Fei, Qing Zhou та Cheng-chi Chao. "Abstract 1538: Analysis of the paired TCRα- and β-V(D)J full-length chains of single-cell sequence from human naïve and antigen-experienced T cells". У Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1538.

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Ohmori, K., H. Chiba, T. Kurosawa, M. Okunishi, K. Ueda та Y. Sato. "Line shapes in the far wings of Hg3P1-1S0 resonance line broadened due to the chemical reactions: Hg∗(3P1)+H2, D2→HgH(X2Σ+,v,j)+H, D". У Proceedings of the 12th International conference on spectral line shapes. AIP, 1995. http://dx.doi.org/10.1063/1.47466.

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Englert, Berthold-Georg, and Kimball A. Milton. "Speeches by V. F. Weisskopf, J. H. Van Vleck, I. I. Rabi, M. Hamermesh, B. T. Feld, R. P. Feynman, and D. Saxon, given in honor of Julian Schwinger at his 60th birthday." In Julian Schwinger Centennial Conference. WORLD SCIENTIFIC, 2019. http://dx.doi.org/10.1142/9789811213144_0019.

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Звіти організацій з теми "V(D)J rearrangement":

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Grant, Stephen G. Increased Illegitimate V(D)J Recombination as a Possible Marker for Breast Cancer Predisposition. Fort Belvoir, VA: Defense Technical Information Center, March 2003. http://dx.doi.org/10.21236/ada423210.

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