Pro pochopení funkce drozofilích adenozin deamináz v organismu, je nutná podrobná analýza mutanta ADGF-A

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60077395%3A_____%2F05%3A00030136" target="_blank" >RIV/60077395:_____/05:00030136 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/60076658:12310/05:00006331

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

A role for adenosine deaminase in Drosophila larval development

Popis výsledku v původním jazyce

Adenosine deaminase is an enzyme present in all organisms that catalyzes the irreversible deamination of adenosine and deoxyadenosine. ADA deficiency in humans causes severe combined immunodeficiency. We have established a Drosophila model to study the effects of altered adenosine levels in vivo by genetic elimination of adenosine deaminase-related growth factor-A, which has ADA activity and is expressed in the gut and hematopoietic organ. The elevated level of adenosine in the hemolymph due to lack ofADGF-A leads to apparently inconsistent phenotypic effects: precocious metamorphic changes including differentiation of macrophage-like cells and fat body disintegration on one hand, and delay of development with block of pupariation on the other. The block of pupariation appears to involve signaling through the adenosine receptor (AdoR), but fat body disintegration, seems to be independent of the AdoR. The existence of such an independent mechanism has also been suggested in mammals.

Název v anglickém jazyce

A role for adenosine deaminase in Drosophila larval development

Popis výsledku anglicky

Adenosine deaminase is an enzyme present in all organisms that catalyzes the irreversible deamination of adenosine and deoxyadenosine. ADA deficiency in humans causes severe combined immunodeficiency. We have established a Drosophila model to study the effects of altered adenosine levels in vivo by genetic elimination of adenosine deaminase-related growth factor-A, which has ADA activity and is expressed in the gut and hematopoietic organ. The elevated level of adenosine in the hemolymph due to lack ofADGF-A leads to apparently inconsistent phenotypic effects: precocious metamorphic changes including differentiation of macrophage-like cells and fat body disintegration on one hand, and delay of development with block of pupariation on the other. The block of pupariation appears to involve signaling through the adenosine receptor (AdoR), but fat body disintegration, seems to be independent of the AdoR. The existence of such an independent mechanism has also been suggested in mammals.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

ED - Fyziologie

OECD FORD obor

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Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2005

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

P L o S Biology

ISSN

1544-9173

e-ISSN

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Svazek periodika

3

Číslo periodika v rámci svazku

7

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

12

Strana od-do

1213-1224

Kód UT WoS článku

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EID výsledku v databázi Scopus

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