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Articles by N Fujimoto
Total Records ( 2 ) for N Fujimoto
  K Harada , H Matsuoka , N Fujimoto , Y Endo , Y Hasegawa , A Matsuo , Y Kikuchi , T Matsumoto and M. Inoue
 

The localization of the type-2 angiotensin II receptor (AT2) in the adrenal glands of rats, guinea pigs, bovines, and humans was examined at the mRNA and protein levels. PCR products for AT2 were detected in the adrenal cortices and adrenal medullae of all the mammals examined with an RT-PCR technique. Three different anti-AT2 antibodies (Abs), whose specificity was confirmed in our hands, recognized a 50-kDa protein in the adrenal glands of the four mammals, and this recognition was abolished by the preabsorption of an Ab with an antigen. Immunoblotting and immunohistochemistry revealed that the 50-kDa protein was expressed consistently and variably in the adrenal cortices and medullae of various mammals, respectively. We conclude that the 50-kDa AT2 is consistently expressed in the adrenal cortex in a wide variety of mammals. (J Histochem Cytochem 58:585–593, 2010)

  M Shiota , A Yokomizo , Y Tada , J Inokuchi , K Tatsugami , K Kuroiwa , T Uchiumi , N Fujimoto , N Seki and S. Naito
 

There are currently few successful therapies for castration-resistant prostate cancer (CRPC). CRPC is thought to result from augmented activation of the androgen/androgen receptor (AR) signaling pathway, which could be enhanced by AR cofactors. In this study, peroxisome proliferator-activated receptor coactivator-1 (PGC-1) was found to be an AR cofactor. PGC-1 interacted with the N-terminal domain of AR, was involved in the N- and C-terminal interaction of AR, and enhanced the DNA-binding ability of AR to androgen-responsive elements in the prostate-specific antigen enhancer and promoter regions to increase the transcription of AR target genes. Silencing of PGC-1 suppressed cell growth of AR-expressing prostate cancer (PCa) cells by inducing cell-cycle arrest at the G1 phase, similar to inhibition of androgen/AR signaling. Furthermore, PGC-1 knock-down also suppressed cell growth in the castration-resistant LNCaP-derivatives. These findings indicate that PGC-1 is involved in the proliferation of AR-expressing PCa cells by acting as an AR coactivator. Modulation of PGC-1 expression or function may offer a useful strategy for developing novel therapeutics for PCa, including CRPC, which depends on AR signaling by overexpressing AR and its coactivators.

 
 
 
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