AID-induced T-lymphoma or B-leukemia/lymphoma in a mouse BMT model. (Q43112724)

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29 January 2020

title

AID-induced T-lymphoma or B-leukemia/lymphoma in a mouse BMT model (English)

1 reference

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29 January 2020

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6

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29 January 2020

author name string

Y Komeno

1

1 reference

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29 January 2020

J Kitaura

2

1 reference

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29 January 2020

N Watanabe-Okochi

3

1 reference

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29 January 2020

N Kato

4

1 reference

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29 January 2020

T Oki

5

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29 January 2020

Y Harada

7

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29 January 2020

H Harada

8

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29 January 2020

R Shinkura

9

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29 January 2020

H Nagaoka

10

1 reference

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29 January 2020

Y Hayashi

11

1 reference

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29 January 2020

T Honjo

12

1 reference

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29 January 2020

T Kitamura

13

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29 January 2020

publication date

1 April 2010

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29 January 2020

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29 January 2020

volume

24

1 reference

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29 January 2020

issue

5

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29 January 2020

page(s)

1018-1024

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https://scigraph.springernature.com/pub.10.1038/leu.2010.40

29 January 2020

exact match

0 references

cites work

Specific expression of activation-induced cytidine deaminase (AID), a novel member of the RNA-editing deaminase family in germinal center B cells

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Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme

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AID mutant analyses indicate requirement for class-switch-specific cofactors

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Separate domains of AID are required for somatic hypermutation and class-switch recombination

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C-terminal deletion of AID uncouples class switch recombination from somatic hypermutation and gene conversion.

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Hypermutation of multiple proto-oncogenes in B-cell diffuse large-cell lymphomas

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Expression of activation-induced cytidine deaminase in human B-cell non-Hodgkin lymphomas

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The B cell mutator AID promotes B lymphoid blast crisis and drug resistance in chronic myeloid leukemia

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AID is required for germinal center-derived lymphomagenesis

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AID expression levels determine the extent of cMyc oncogenic translocations and the incidence of B cell tumor development

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Constitutive expression of AID leads to tumorigenesis

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Organ-specific profiles of genetic changes in cancers caused by activation-induced cytidine deaminase expression

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Tissue-specific sensitivity to AID expression in transgenic mouse models.

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Negative regulation of activation-induced cytidine deaminase in B cells

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Restricting activation-induced cytidine deaminase tumorigenic activity in B lymphocytes

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Plat-E: an efficient and stable system for transient packaging of retroviruses

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AML1 mutations induced MDS and MDS/AML in a mouse BMT model

21 January 2018

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Mutations of the BCL6 proto-oncogene disrupt its negative autoregulation in diffuse large B-cell lymphoma.

21 January 2018

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The very 5' end and the constant region of Ig genes are spared from somatic mutation because AID does not access these regions

21 January 2018

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Notch signaling in leukemia

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Genome-wide analysis of genetic alterations in acute lymphoblastic leukaemia

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AID is required for c-myc/IgH chromosome translocations in vivo

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Balancing AID and DNA repair during somatic hypermutation

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The stability of AID and its function in class-switching are critically sensitive to the identity of its nuclear-export sequence

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FBW7 mutations in leukemic cells mediate NOTCH pathway activation and resistance to gamma-secretase inhibitors

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BCR–ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros

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Helicobacter pylori infection triggers aberrant expression of activation-induced cytidine deaminase in gastric epithelium

21 January 2018

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inferred from DOI database lookup

7 January 2021

based on heuristic

Retrovirus-mediated gene transfer and expression cloning: powerful tools in functional genomics

1 reference

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inferred from DOI database lookup

7 January 2021

based on heuristic

Chromosomal translocations cause deregulated BCL6 expression by promoter substitution in B cell lymphoma.

1 reference

https://api.crossref.org/works/10.1038%2FLEU.2010.40