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  • 1
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] The protein tyrosine phosphatase SHP-1 is a well-known inhibitor of activation-promoting signaling cascades in hematopoietic cells but its potential role in insulin target tissues is unknown. Here we show that Ptpn6me-v/me-v (also known as viable motheaten) mice bearing a functionally deficient ...
    Type of Medium: Electronic Resource
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  • 2
    Publication Date: 2020-02-06
    Description: Orbital forcing influences climate phenomena by changing incoming solar radiation in season and latitude. Here, changes in the El Niño-Southern Oscillation (ENSO)’s impact on the East Asian winter monsoon (EAWM) due to orbital forcing, especially for three selected time periods in each of two interglacial periods, the Eemian (126, 122, 115 ka) and Holocene (9, 6, 0 ka), are investigated. There was a high negative correlation between ENSO and EAWM when the obliquity was low, the processional angle was large, and especially when accompanied by large eccentricity, which corresponds to a weaker monsoon period. The correlation was also high when ENSO variability was high, which interestingly corresponded to lower obliquity and higher-degree precession periods. Therefore, as both lower obliquity and higher-degree precession, such as during 115 ka and 0 ka, cause the EAWM to be weakened through higher winter insolation over Northern hemisphere, and the ENSO to be enhanced through an intensified zonal contrast of the equatorial sea surface temperature, the relationship between the ENSO and EAWM becomes tighter. The opposite case (i.e., during 126 and 9 ka) is also true dynamically. Furthermore, the sensitivity of boreal winter precipitation against sea surface temperature (SST) anomaly over the tropical Pacific, which depends on mean SST, was positively correlated to the strength of the ENSO-EAWM correlation, implying that the warmer mean ocean surface causes the strong response of atmosphere to change in the SST anomaly, thereby enhancing the impact of ENSO on EAWM. Warmer wintertime tropical SST is attributed to higher insolation over the tropics, especially during 115 and 0 ka, while cooler SSTs occurred during 126 and 9 ka.
    Type: Article , PeerReviewed
    Format: text
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  • 3
    Publication Date: 2014-07-31
    Description: Background: The essential oil of Pinus koraiensis (EOPK) is biologically active compound obtained from the leaves of P. koraiensis. The goal of this study was to investigate the anti-cancer mechanism of EOPK in HCT116 colorectal cancer cells. Methods: HCT116 cell proliferation was assessed by conducting crystal violet and BrdU assays. To assess the effects of EOPK on cell migration, we performed a wound-healing assay. Further, the contribution of PAK1 to EOPK-induced AKT and extracellular signal-regulated kinase (ERK) suppression was assessed by siRNA-mediated PAK1 knockdown. Changes to the expression and phosphorylation of PAK1 and its effectors were determined by western blotting, and changes to the actin cytoskeleton were determined by performing an immunofluorescence assay. Results: EOPK significantly decreased HCT116 cell proliferation and migration, and induced G1 arrest without affecting normal cells. Additionally, EOPK suppressed the expression of PAK1, and decreased ERK and AKT phosphorylation in HCT116 cells. Finally, EOPK suppressed beta-catenin, cyclin D1, and CDK4/6 expression. Conclusions: Our studies indicate that EOPK significantly reduced proliferation and migration of colorectal cancer cells. Furthermore, EOPK suppressed PAK1 expression in a dose-dependent manner, and this suppression of PAK1 led to inhibition of ERK, AKT, and beta-catenin activities. Our findings suggest that EOPK exerts its anticancer activity via the inhibition of PAK1 expression, suggesting it may be a potent chemotherapeutic agent for colorectal cancer.
    Electronic ISSN: 1472-6882
    Topics: Medicine
    Published by BioMed Central
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  • 4
    Publication Date: 2013-11-23
    Description: Pin1, a conserved eukaryotic Peptidyl-prolyl cis / trans isomerase, has profound effects on numerous key-signaling molecules, and its deregulation contributes to disease, particularly cancer. Although Pin1-mediated prolyl isomerization is an essential and novel regulatory mechanism for protein phosphorylation, little is known about the upstream signaling pathway(s) that regulates Pin1 activity. Here, we identify MAP3K-related serine–threonine kinase (the gene encoding COT/Tpl2) as a kinase responsible for phosphorylation of Pin1 Ser16. COT interacts with and phosphorylates Pin1 on Ser16. Consequently, Pin1 Ser16 phosphorylation by COT increases cyclin D1 abundance and enhances tumorigenecity of MCF7 cells. In contrast, depletion of COT in MCF7 cells leads to downregulation of Pin1 Ser16 phosphorylation, which subsequently decrease cyclin D1 levels, inhibiting tumorigenecity of MCF7 cells. In a xenograft model, treatment of TKI, a COT inhibitor, and Juglone, a Pin1 inhibitor, abrogates tumor growth. In human breast cancer patients, immunohistochemical staining shows that Pin1 pSer16 levels are positively correlated with COT levels, providing strong evidence for an essential role of the COT/Pin1 axis in conveying oncogenic signals to promote aggressiveness in human breast cancer. © 2013 Wiley Periodicals, Inc.
    Print ISSN: 0899-1987
    Electronic ISSN: 1098-2744
    Topics: Medicine
    Published by Wiley-Blackwell
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  • 5
    Publication Date: 2012-05-02
    Description: Pin1 is a unique regulator that catalyzes the conversion of a specific phospho-Ser/Thr-Pro-containing motif in target proteins. Herein, we identified AMP-activated protein kinase (AMPK) as a Pin1-binding protein. Pin1 wild-type, but not Pin1 mutant at serine 16 (S16A), associated with AMPK. Reciprocally, the constitutively active form of AMPK (AMPK-CA), but not the dominant negative form of AMPK (AMPK-DN), interacted with Pin1 wild type. In addition, mutation of Ser176 site in AMPK led to a significant loss of binding between AMPK and Pin1. Ablation of the Pin1 gene in MEFs enhanced AMPK phosphorylation induced by AICAR. Pin1 overexpression in Pin1 −/− MEFs and SK-HEP-1 cells attenuated AMPK phosphorylation induced by EGF, whereas gene knockdown of Pin1 by siRNA enhanced it. The association between Pin1 and AMPK was increased by EGF, leading to their interaction with protein phosphatase-2A (PP2A). Furthermore, Pin1 increased the PP2A activity induced by EGF. In addition, AMPK-WT and AMPK-CA, but not AMPK-DN, inhibited EGF-induced neoplastic cell transformation of JB6 Cl41 cells and tumorigenicity of SK-HEP-1 cells. The overexpression of Pin1 in JB6 Cl41 cells and SK-HEP-1 cells attenuated the inhibitory effect of AMPK in EGF-induced neoplastic cell transformation of JB6 Cl41 and tumorigenicity of SK-HEP-1 cells, respectively. Taken together, these results indicate that Pin1 plays a pivotal role in EGF-induced carcinogenesis through downregulation of AMPK activity in hepatocarcinoma cells. © 2012 Wiley Periodicals, Inc.
    Print ISSN: 0899-1987
    Electronic ISSN: 1098-2744
    Topics: Medicine
    Published by Wiley-Blackwell
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