Matches in SemOpenAlex for { <https://semopenalex.org/work/W2566743224> ?p ?o ?g. }
Showing items 1 to 66 of
66
with 100 items per page.
- W2566743224 abstract "In the previous work, a minimal region of recurrent deletion distal to the Tp53 gene was identified in BDII rat model for endometrial adenocarcinoma and the MYO1C gene was singled out as the tumor suppressor candidate in this region. Myo1c can bind to PIP2, the substrate of PI3-kinase, as well as to the mTOR complex, indicating a role for MYO1C in the PI3-kinase pathway. In this study, we assessed protein levels of 12 members of PI3-kinase/AKT signaling pathways in transient transfected HeLa cells expressing increasing amounts of MYO1C using Western blotting and densitometry analyses. Results revealed decreased protein levels of PTEN, AKT, and phosphorylated AKT, at both residues T308 and S473, and an increased expression of p110α protein in the cells transfected with the MYO1C gene expression constructs compared to the control cells transfected with empty plasmid. We next investigated potential effect of MYO1C protein depletion on serum-induced activation (phosphorylation) of AKT in the MCF10A cells that has de novo expression of MYO1C protein. Following serum stimulation, AKT was rapidly phosphorylated in its residue S473 (pAKTS473) in the cells transfected with MYO1C-siRNA, but with significantly lesser extent in the control cells. Overall, a negative correlation between the protein expression of MYO1C and AKT expression/activation was suggested, signifying a role for MYO1C as a negative regulator of PI3-kinsase/AKT signaling pathway. This is in agreement with the initial hypothesis of involvement of MYO1C in tumorigenesis pathways through its potential tumor suppressor activity. Further studies are required to fully understand the functional contribution of MYO1C to tumor development. Citation Format: Kittichate Visuttijai, Katarina Ejeskar, Afrouz Behboudi. Analyses of protein expression of PI 3-kinase/AKT signaling in response to altered expression of motor protein MYO1C. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2166. doi:10.1158/1538-7445.AM2015-2166" @default.
- W2566743224 created "2017-01-06" @default.
- W2566743224 creator A5059264497 @default.
- W2566743224 creator A5061536229 @default.
- W2566743224 creator A5067630005 @default.
- W2566743224 date "2015-08-01" @default.
- W2566743224 modified "2023-09-27" @default.
- W2566743224 title "Abstract 2166: Analyses of protein expression of PI 3-kinase/AKT signaling in response to altered expression of motor protein MYO1C" @default.
- W2566743224 doi "https://doi.org/10.1158/1538-7445.am2015-2166" @default.
- W2566743224 hasPublicationYear "2015" @default.
- W2566743224 type Work @default.
- W2566743224 sameAs 2566743224 @default.
- W2566743224 citedByCount "0" @default.
- W2566743224 crossrefType "proceedings-article" @default.
- W2566743224 hasAuthorship W2566743224A5059264497 @default.
- W2566743224 hasAuthorship W2566743224A5061536229 @default.
- W2566743224 hasAuthorship W2566743224A5067630005 @default.
- W2566743224 hasConcept C104317684 @default.
- W2566743224 hasConcept C11960822 @default.
- W2566743224 hasConcept C153911025 @default.
- W2566743224 hasConcept C184235292 @default.
- W2566743224 hasConcept C54009773 @default.
- W2566743224 hasConcept C54355233 @default.
- W2566743224 hasConcept C62478195 @default.
- W2566743224 hasConcept C75217442 @default.
- W2566743224 hasConcept C86554907 @default.
- W2566743224 hasConcept C86803240 @default.
- W2566743224 hasConcept C95444343 @default.
- W2566743224 hasConceptScore W2566743224C104317684 @default.
- W2566743224 hasConceptScore W2566743224C11960822 @default.
- W2566743224 hasConceptScore W2566743224C153911025 @default.
- W2566743224 hasConceptScore W2566743224C184235292 @default.
- W2566743224 hasConceptScore W2566743224C54009773 @default.
- W2566743224 hasConceptScore W2566743224C54355233 @default.
- W2566743224 hasConceptScore W2566743224C62478195 @default.
- W2566743224 hasConceptScore W2566743224C75217442 @default.
- W2566743224 hasConceptScore W2566743224C86554907 @default.
- W2566743224 hasConceptScore W2566743224C86803240 @default.
- W2566743224 hasConceptScore W2566743224C95444343 @default.
- W2566743224 hasLocation W25667432241 @default.
- W2566743224 hasOpenAccess W2566743224 @default.
- W2566743224 hasPrimaryLocation W25667432241 @default.
- W2566743224 hasRelatedWork W1510472405 @default.
- W2566743224 hasRelatedWork W1821475189 @default.
- W2566743224 hasRelatedWork W2005408848 @default.
- W2566743224 hasRelatedWork W2011468770 @default.
- W2566743224 hasRelatedWork W2036084453 @default.
- W2566743224 hasRelatedWork W2047938509 @default.
- W2566743224 hasRelatedWork W2074079253 @default.
- W2566743224 hasRelatedWork W2074163964 @default.
- W2566743224 hasRelatedWork W2075175079 @default.
- W2566743224 hasRelatedWork W2077371239 @default.
- W2566743224 hasRelatedWork W2084980348 @default.
- W2566743224 hasRelatedWork W2106047706 @default.
- W2566743224 hasRelatedWork W2109180697 @default.
- W2566743224 hasRelatedWork W2144216187 @default.
- W2566743224 hasRelatedWork W2176346661 @default.
- W2566743224 hasRelatedWork W2313888290 @default.
- W2566743224 hasRelatedWork W2388634495 @default.
- W2566743224 hasRelatedWork W2434957940 @default.
- W2566743224 hasRelatedWork W2794038510 @default.
- W2566743224 hasRelatedWork W3092617992 @default.
- W2566743224 isParatext "false" @default.
- W2566743224 isRetracted "false" @default.
- W2566743224 magId "2566743224" @default.
- W2566743224 workType "article" @default.