Systematic analysis of BCR-ABL interactome in chronic myeloid
leukemia

a 2017

Systematic analysis of BCR-ABL interactome in chronic myeloid leukemia

GREGOR, Tomáš, Jan RYNEŠ, Silvie TRANTÍRKOVÁ, Jiří MAYER, Pavel KREJČÍ et. al.

Základní údaje

Originální název

Systematic analysis of BCR-ABL interactome in chronic myeloid leukemia

Autoři

GREGOR, Tomáš (203 Česká republika, domácí), Jan RYNEŠ (203 Česká republika, domácí), Silvie TRANTÍRKOVÁ (203 Česká republika, domácí), Jiří MAYER (203 Česká republika, domácí), Pavel KREJČÍ (203 Česká republika, domácí) a Lukáš TRANTÍREK (203 Česká republika, domácí)

Vydání

42nd Congress of the Federation-of-European-Biochemical-Societies (FEBS) on From Molecules to Cells and Back, 2017

Další údaje

Jazyk

angličtina

Typ výsledku

Konferenční abstrakt

Obor

10608 Biochemistry and molecular biology

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Impakt faktor

Impact factor: 4.530

Kód RIV

RIV/00216224:14740/17:00095713

Organizační jednotka

Středoevropský technologický institut

ISSN

UT WoS

000409918903263

Klíčová slova anglicky

BCR-ABL; chronic myeloid leukemia

Štítky

rivok

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 19. 3. 2018 17:00, Mgr. Pavla Foltynová, Ph.D.

Anotace

V originále

Chronic myeloid leukemia (CML) is a myeloproliferative cancer that is caused by “Philadelphia chromosome” translocation that results in a formation of fusion protein BCR-ABL. This constitutively active tyrosine kinase is necessary and sufficient to cause CML. Several small molecule tyrosine kinase inhibitors (TKI) targeting BCR-ABL kinase activity had been developed and greatly improved CML prognosis. However, significant number of patients develops resistance to TKIs and relapse. Growing evidence shows the importance of other BCR-ABL interaction partners in CML pathogenesis. Precise elucidation of the interactome can lead to design of conceptually new drug targeting different pathways and overcoming TKI resistance. One of our goals is to elucidate precise binding interface among BCR-ABL and it’s “core complex” interaction partners. Our approach involves use of peptide microarrays, which allow us to map the binding interface with single amino acid resolution. Binding motifs discovered in unstructured parts of BCR-ABL can be used to generate synthetic peptide abolishing particular protein interaction. Furthermore, we created large pallet of BCR-ABL deletion/substitution mutants in order to verify interaction boundaries and co-immunoprecipitation experiments have yielded potential new binding sites for some of the core complex interactors.

Návaznosti

LQ1601, projekt VaV

Název: CEITEC 2020 (Akronym: CEITEC2020)

Investor: Ministerstvo školství, mládeže a tělovýchovy ČR, CEITEC 2020

NV15-33232A, projekt VaV

Název: Identifikace nových možností léčby achondroplásie prostřednictvím analýzy interakce FGFR3 a adaptérového proteinu Frs2

NV15-34405A, projekt VaV

Název: Identifikace nových možností léčby chronické myeloidní leukémie pomocí systematické analýzy interaktomu proteinu BCR-ABL

Citovat

GREGOR, Tomáš, Jan RYNEŠ, Silvie TRANTÍRKOVÁ, Jiří MAYER, Pavel KREJČÍ a Lukáš TRANTÍREK. Systematic analysis of BCR-ABL interactome in chronic myeloid leukemia. In 42nd Congress of the Federation-of-European-Biochemical-Societies (FEBS) on From Molecules to Cells and Back. 2017. ISSN 1742-464X.

@proceedings{1411821,
   author = {Gregor, Tomáš and Ryneš, Jan and Trantírková, Silvie and Mayer, Jiří and Krejčí, Pavel and Trantírek, Lukáš},
   booktitle = {42nd Congress of the Federation-of-European-Biochemical-Societies (FEBS) on From Molecules to Cells and Back},
   keywords = {BCR-ABL; chronic myeloid leukemia},
   language = {eng},
   title = {Systematic analysis of BCR-ABL interactome in chronic myeloid leukemia},
   url = {https://2017.febscongress.org/abstract_preview.aspx?idAbstractEnc=4424170093097092096093424170},
   year = {2017}
}

TY  - CONF
ID  - 1411821
AU  - Gregor, Tomáš - Ryneš, Jan - Trantírková, Silvie - Mayer, Jiří - Krejčí, Pavel - Trantírek, Lukáš
PY  - 2017
TI  - Systematic analysis of BCR-ABL interactome in chronic myeloid leukemia
KW  - BCR-ABL
KW  - chronic myeloid leukemia
UR  - https://2017.febscongress.org/abstract_preview.aspx?idAbstractEnc=4424170093097092096093424170
L2  - https://2017.febscongress.org/abstract_preview.aspx?idAbstractEnc=4424170093097092096093424170
N2  - Chronic myeloid leukemia (CML) is a myeloproliferative cancer that is caused by “Philadelphia chromosome” translocation that results in a formation of fusion protein BCR-ABL. This constitutively active tyrosine kinase is necessary and sufficient to cause CML. Several small molecule tyrosine kinase inhibitors (TKI) targeting BCR-ABL kinase activity had been developed and greatly improved CML prognosis. However, significant number of patients develops resistance to TKIs and relapse. Growing evidence shows the importance of other BCR-ABL interaction partners in CML pathogenesis. Precise elucidation of the interactome can lead to design of conceptually new drug targeting different pathways and overcoming TKI resistance. One of our goals is to elucidate precise binding interface among BCR-ABL and it’s “core complex” interaction partners. Our approach involves use of peptide microarrays, which allow us to map the binding interface with single amino acid resolution. Binding motifs discovered in unstructured parts of BCR-ABL can be used to generate synthetic peptide abolishing particular protein interaction. Furthermore, we created large pallet of BCR-ABL deletion/substitution mutants in order to verify interaction boundaries and co-immunoprecipitation experiments have yielded potential new binding sites for some of the core complex interactors.
ER  -

GREGOR, Tomáš, Jan RYNEŠ, Silvie TRANTÍRKOVÁ, Jiří MAYER, Pavel KREJČÍ a Lukáš TRANTÍREK. Systematic analysis of BCR-ABL interactome in chronic myeloid leukemia. In \textit{42nd Congress of the Federation-of-European-Biochemical-Societies (FEBS) on From Molecules to Cells and Back}. 2017. ISSN~1742-464X.

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