Interaction of hookworm 14-3-3 with the forkhead transcription factor DAF-16 requires intact Akt phosphorylation sites.
Interaction of hookworm 14-3-3 with the forkhead transcription factor DAF-16 requires intact Akt phosphorylation sites.
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钩虫 14-3-3 与叉头转录因子 DAF-16 的相互作用需要完整的 Akt 磷酸化位点。
DOI：
10.1186/1756-3305-2-21
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发表时间：
2009-04-24
影响因子：
3.2
通讯作者：
Hawdon JM
中科院分区：
文献类型：
--
作者：
Kiss JE;Gao X;Krepp JM;Hawdon JM
Third-stage infective larvae (L3) of hookworms are in an obligatory state of developmental arrest that ends upon entering the definitive host, where they receive a signal that re-activates development. Recovery from the developmentally arrested dauer stage of Caenorhabditis elegans is analogous to the resumption of development during hookworm infection. Insulin-like signaling (ILS) mediates recovery from arrest in C. elegans and activation of hookworm dauer L3. In C. elegans, phosphorylation of the forkhead transcription factor DAF-16 in response to ILS creates binding cites for the 14-3-3 protein Ce-FTT-2, which translocates DAF-16 out of the nucleus, resulting in resumption of reproductive development. To determine if hookworm 14-3-3 proteins play a similar role in L3 activation, hookworm FTT-2 was identified and tested for its ability to interact with A. caninum DAF-16 in vitro. The Ac-FTT-2 amino acid sequence was 91% identical to the Ce-FTT-2, and was most closely related to FTT-2 from other nematodes. Ac-FTT-2 was expressed in HEK 293T cells, and was recognized by an antibody against human 14-3-3β isoform. Reciprocal co-immunoprecipitations using anti-epitope tag antibodies indicated that Ac-FTT-2 interacts with Ac-DAF-16 when co-expressed in serum-stimulated HEK 293T cells. This interaction requires intact Akt consensus phosphorylation sites at serine107 and threonine312, but not serine381. Ac-FTT-2 was undetectable by Western blot in excretory/secretory products from serum-stimulated (activated) L3 or adult A. caninum. The results indicate that Ac-FTT-2 interacts with DAF-16 in a phosphorylation-site dependent manner, and suggests that Ac-FTT-2 mediates activation of L3 by binding Ac-DAF-16 during hookworm infection.
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影响因子：
1.3
作者：
Basso, W;Venturini, L;Dubey, JP
通讯作者：
Dubey, JP
影响因子：
3.9
作者：
Andrade, MA;Siles-Lucas, M;Muro, A
通讯作者：
Muro, A
影响因子：
1.5
作者：
Cappello, M;Hawdon, JM;Hotez, PJ
通讯作者：
Hotez, PJ
影响因子：
2.4
作者：
Craig, H;Wastling, JM;Knox, DP
通讯作者：
Knox, DP
影响因子：
4
作者：
Brand, AM;Varghese, G;Hawdon, JM
通讯作者：
Hawdon, JM