(Q44081409)

29 November 2017

title

Selective apoptosis of tandemly duplicated FLT3-transformed leukemia cells by Hsp90 inhibitors (English)

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29 November 2017

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Y Minami

1

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29 November 2017

H Kiyoi

2

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29 November 2017

Y Yamamoto

3

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29 November 2017

K Yamamoto

4

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29 November 2017

R Ueda

5

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29 November 2017

H Saito

6

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29 November 2017

T Naoe

7

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29 November 2017

publication date

1 August 2002

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29 November 2017

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29 November 2017

volume

16

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29 November 2017

issue

8

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29 November 2017

page(s)

1535-1540

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https://scigraph.springernature.com/pub.10.1038/sj.leu.2402558

29 November 2017

exact match

0 references

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Molecular cloning of a ligand for the flt3/flk-2 tyrosine kinase receptor: a proliferative factor for primitive hematopoietic cells

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Internal tandem duplication of the FLT3 gene is preferentially seen in acute myeloid leukemia and myelodysplastic syndrome among various hematological malignancies. A study on a large series of patients and cell lines

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Internal tandem duplication of FLT3 associated with leukocytosis in acute promyelocytic leukemia. Leukemia Study Group of the Ministry of Health and Welfare (Kohseisho)

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Biological characteristics and prognosis of adult acute myeloid leukemia with internal tandem duplications in the Flt3 gene

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Internal tandem duplication of the FLT3 gene is a novel modality of elongation mutation which causes constitutive activation of the product

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Tandem-duplicated Flt3 constitutively activates STAT5 and MAP kinase and introduces autonomous cell growth in IL-3-dependent cell lines

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https://api.crossref.org/works/10.1038%2FSJ.LEU.2402558

7 January 2021

In vivo treatment of mutant FLT3-transformed murine leukemia with a tyrosine kinase inhibitor

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Inhibition of transforming activity of tyrosine kinase oncogenes by herbimycin A.

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Inhibition of heat shock protein HSP90-pp60v-src heteroprotein complex formation by benzoquinone ansamycins: essential role for stress proteins in oncogenic transformation

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Polyubiquitination and proteasomal degradation of the p185c-erbB-2 receptor protein-tyrosine kinase induced by geldanamycin

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https://api.crossref.org/works/10.1038%2FSJ.LEU.2402558

7 January 2021

Disruption of the Raf-1-Hsp90 Molecular Complex Results in Destabilization of Raf-1 and Loss of Raf-1-Ras Association

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Crystal structure of an Hsp90-geldanamycin complex: targeting of a protein chaperone by an antitumor agent

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7 January 2021

Geldanamycin as a potential anti-cancer agent: its molecular target and biochemical activity

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7 January 2021

Role of the heat shock response and molecular chaperones in oncogenesis and cell death

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7 January 2021

The function of steroid hormone receptors is inhibited by the hsp90-specific compound geldanamycin

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7 January 2021

The Hsp90 inhibitor geldanamycin selectively sensitizes Bcr-Abl-expressing leukemia cells to cytotoxic chemotherapy

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7 January 2021

Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies

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7 January 2021

Antibiotic radicicol binds to the N-terminal domain of Hsp90 and shares important biologic activities with geldanamycin

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7 January 2021

Targeting of the protein chaperone, HSP90, by the transformation suppressing agent, radicicol

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7 January 2021

Hsp90 as a capacitor for morphological evolution

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Suppression of interleukin-3-induced gene expression by a C-terminal truncated Stat5: role of Stat5 in proliferation.

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7 January 2021

Targeted disruption of the flk2/flt3 gene leads to deficiencies in primitive hematopoietic progenitors

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https://api.crossref.org/works/10.1038%2FSJ.LEU.2402558

7 January 2021

Identifiers

DOI

10.1038/SJ.LEU.2402558

1 reference

29 November 2017

1 reference