Ribosomal Protein S6 Kinases, 70-kDa

Publication Title: 
PloS One

BACKGROUND: Recent studies have demonstrated that activation of autophagy increases the lifespan of organisms from yeast to flies. In contrast to the lifespan extension effect in lower organisms, it has been reported that overexpression of unc-51-like kinase 3 (ULK3), the mammalian homolog of autophagy-specific gene 1 (ATG1), induces premature senescence in human fibroblasts. Therefore, we assessed whether the activation of autophagy would genuinely induce premature senescence in human cells.

Author(s): 
Kang, Hyun Tae
Lee, Ki Baek
Kim, Sung Young
Choi, Hae Ri
Park, Sang Chul
Publication Title: 
Biochemical and Biophysical Research Communications

Cellular senescence is a tumor suppression mechanism. We previously reported that CKII downregulation induces senescence in human lung fibroblast IMR-90 and colon cancer HCT116 cells. In this study, potential longevity drugs, including rapamycin, vitamin C, and vitamin E, blocked CKII downregulation-mediated senescence through reduction of reactive oxygen species (ROS) production in HCT116 cells.

Author(s): 
Park, Ji Hye
Kim, Jin Joo
Bae, Young-Seuk
Publication Title: 
Aging Cell

Dietary restriction (DR) results in a robust increase in lifespan while maintaining the physiology of much younger animals in a wide range of species. Here, we examine the role of drr-2, a DR-responsive gene recently identified, in determining the longevity of Caenorhabditis elegans. Inhibition of drr-2 has been shown to increase longevity. However, the molecular mechanisms by which drr-2 influences longevity remain unknown.

Author(s): 
Ching, Tsui-Ting
Paal, Alisha B.
Mehta, Avni
Zhong, Linda
Hsu, Ao-Lin
Publication Title: 
Cardiovascular Research

OBJECTIVE: We have previously demonstrated that nuclear factor kappa B (NFkappaB) activation is needed for the development of cardiac hypertrophy in vivo. NFkappaB is a downstream transcription factor in the Toll-like receptor (TLR)-mediated signaling pathway; therefore, we investigated a role of TLR4 in cardiac hypertrophy in vivo. METHODS: TLR4-deficient mice (C.C3H-Tlr4(lps-d), n = 6), wild-type (WT) genetic background mice (BALB/c, n = 6), TLR4-deleted strain (C57BL/10ScCr, n = 8), and WT controls (C57BL/10ScSn, n = 8) were subjected to aortic banding for 2 weeks.

Author(s): 
Ha, Tuanzhu
Li, Yuehua
Hua, Fang
Ma, Jinag
Gao, Xiang
Kelley, Jim
Zhao, Aiqiu
Haddad, Georges E.
Williams, David L.
William Browder, I.
Kao, Race L.
Li, Chuanfu
Publication Title: 
Cancer Research

Understanding the molecular basis and target of traditional medicine is critical for drug development. Celastrol, derived from Trypterygium wilfordii Hook F. ("Thunder of God Vine"), a traditional Chinese medicine plant, has been assigned anticancer activities, but its mechanism is not well understood. Here, we investigated whether Celastrol could inhibit angiogenesis-mediated tumor growth and, if so, through what mechanism. When given s.c.

Author(s): 
Pang, Xiufeng
Yi, Zhengfang
Zhang, Jing
Lu, Binbin
Sung, Bokyung
Qu, Weijing
Aggarwal, Bharat B.
Liu, Mingyao
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