Archives
- 2025-10
- 2025-09
- 2025-03
- 2025-02
- 2025-01
- 2024-12
- 2024-11
- 2024-10
- 2024-09
- 2024-08
- 2024-07
- 2024-06
- 2024-05
- 2024-04
- 2024-03
- 2024-02
- 2024-01
- 2023-12
- 2023-11
- 2023-10
- 2023-09
- 2023-08
- 2023-07
- 2023-06
- 2023-05
- 2023-04
- 2023-03
- 2023-02
- 2023-01
- 2022-12
- 2022-11
- 2022-10
- 2022-09
- 2022-08
- 2022-07
- 2022-06
- 2022-05
- 2022-04
- 2022-03
- 2022-02
- 2022-01
- 2021-12
- 2021-11
- 2021-10
- 2021-09
- 2021-08
- 2021-07
- 2021-06
- 2021-05
- 2021-04
- 2021-03
- 2021-02
- 2021-01
- 2020-12
- 2020-11
- 2020-10
- 2020-09
- 2020-08
- 2020-07
- 2020-06
- 2020-05
- 2020-04
- 2020-03
- 2020-02
- 2020-01
- 2019-12
- 2019-11
- 2019-10
- 2019-09
- 2019-08
- 2019-07
- 2018-07
-
ZM 447439 br A Rs which were cloned and then pharmacological
2024-07-29
A3Rs, which were cloned and then pharmacologically identified in the early 1990s, are expressed in multiple organs and peripheral tissues including ZM 447439 involved in inflammatory responses (Gessi et al., 2008, Borea et al., 2014). While low levels are expressed in the CNS, A3R agonists produce
-
A key step in the ADAR
2024-07-29
A key step in the ADAR reaction is the formation of the adenosine covalent hydrate with a tetrahedral center at C6. The nucleoside analog 8-azanebularine (box in Fig. 6), with its relatively high propensity to form a covalent hydrate, is useful as an adenosine replacement in ADAR2 substrates to trap
-
Finally we show that the optimal
2024-07-29
Finally, we show that the optimal corporate tax rate is strictly positive, balancing the increase in tax revenues against the loss in consumer surplus due to higher prices and fewer firms (products). This result is related to the well-known “excessive entry theorem” that shows, for a large class of
-
Since the localization of LO depends on
2024-07-29
Since the localization of 5-LO depends on phosphorylation, we also analyzed the phosphorylation profile of 5-LO-WT and all isoforms by Western blot using specific Curcumol receptor against the phosphorylation sites S271 and S523. Whereas phosphorylation at S271 activates the 5-LO, inhibits nuclear e
-
br Author contributions br Acknowledgments TJC KW and
2024-07-26
Author contributions Acknowledgments TJC, KW, and VG are supported by awards made to MJN: a Consolidator Grant from the European Research Council under Grant no. 311336; a University Research Fellowship from the Royal Society, and a Career Development Award from the Human Frontiers Science Pro
-
Findings of the present study provide
2024-07-26
Findings of the present study provide a molecular mechanism for the elevated ASK1 expression in obesity and how it may be functionally linked to whole-body insulin resistance. The role our findings assign to increased E2F1 in upregulating ASK1 parallels the capacity of this transcription factor to r
-
br Regulatory mechanisms of ASK activity br
2024-07-26
Regulatory mechanisms of ASK1 activity The functions of ASK1 in disease ASK1 inhibitor As mentioned above, ASK1 plays a pivotal role in the pathogenesis of various diseases; hence, an ASK1 inhibitor has therapeutic potential. Although inhibitors of the ASK1 downstream kinases p38 and JNK ar
-
It has been proven that genetic polymorphisms can play an
2024-07-26
It has been proven that genetic polymorphisms can play an important role in development of hypertension and CVDs. In a Turkish population-based study, it was found that the APLNR gene (rs948847-A445C) polymorphism was not associated with coronary artery disease (CAD), but it was shown to be related
-
According to the present observations the
2024-07-26
According to the present observations, the Ampkα1 isoform promotes AP-1 transcriptional activity and thereby fosters 73122 of AP-1 target genes in cardiomyocytes via activation of Pkcζ. The transcription factor AP-1 plays a decisive role during cardiac remodeling [24], [25], [26], [37]. AP-1 modula
-
The lack of benefit in
2024-07-26
The lack of benefit in terms of overall survival for antiangiogenic treatment was similar when antiangiogenic drug was used both as first and second-line therapy, and both in association with cytotoxic treatment or alone. Noteworthy, a trend for an inferior outcome was observed in the group of patie
-
Immunohistochemistry in tissue samples showed the
2024-07-26
Immunohistochemistry in tissue samples showed the expression of several nuclear receptor co-activators, including NCOA1, NCOA2, NCOA3, CREBBP, and EP300, in 85–100% of Fmoc-Phe-OH tumors even some of which lacked AR expression (Boorjian et al., 2009). Knockdown of each co-activator also resulted in
-
Inhibition of autophagy has been shown to
2024-07-26
Inhibition of autophagy has been shown to alleviate neuronal damage after cerebral ischemia, both in cell culture and rodent models (Koike et al., 2008, Li et al., 2015, Wang et al., 2016, Zhang et al., 2014, Zheng et al., 2014). Therefore, blockage of autophagy is a potential target for prevention
-
Thonzonium Bromide Data used in preparation of this article
2024-07-26
Data used in preparation of this article were obtained from the ADNI database (adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing o
-
In conclusion phenolic hydroxyl was introduced not only
2024-07-26
In conclusion, phenolic hydroxyl was introduced not only to C3 side chain but also to C6 or C7 position of the quinoxalinone core, resulting in a new group of ARIs candidates exhibiting antioxidant activity. Biological activity tests suggested that compounds were not only sufficient to inhibit ALR2
-
A straightforward synthetic pathway was
2024-07-26
A straightforward synthetic pathway was adopted to synthesize the target compounds as outlined in . The starting chloromethylquinazolinones (–) were synthesized from anthranilic H-9 dihydrochloride synthesis in two steps following reported procedures., , , The first step involves chloroacetylation
15074 records 102/1005 page Previous Next First page 上5页 101102103104105 下5页 Last page