New era for ME/CFS research as top cytokine study attracts media headlines
The immune systems of patients who have recently developed ME/CFS look markedly different from those who have been ill for much longer, according to a major new study from Drs. Ian Lipkin and Mady Hornig at Columbia University. This shift in immune function hadn’t been seen before.
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Xmrv creb and prostate cancer

Discussion in 'XMRV Research and Replication Studies' started by Gerwyn, May 4, 2010.

  1. Gerwyn

    Gerwyn Guest

    XMRV can alter the function of CREB.CREB function is abnormal in patients with prostate cancer.XMRV has been found integrated within the creb gene in patients with prostate cancer


    Targeting CREB for Cancer Therapy: Friend or Foe

    Authors: Xiao, X.; Li, B.X.; Mitton, B.; Ikeda, A.; Sakamoto, K.M.

    Source: Current Cancer Drug Targets, Volume 10, Number 4, June 2010 , pp. 384-391(8)

    Publisher: Bentham Science Publishers




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    More about this publication?

    * Current Cancer Drug Targets aims to cover all the latest and outstanding developments on the medicinal chemistry, pharmacology, molecular biology, genomics and biochemistry of contemporary molecular drug targets involved in cancer, e.g. disease speci... more
    Current Cancer Drug Targets aims to cover all the latest and outstanding developments on the medicinal chemistry, pharmacology, molecular biology, genomics and biochemistry of contemporary molecular d

    Abstract:
    The cyclic-AMP response element-binding protein (CREB) is a nuclear transcription factor activated by phosphorylation at Ser133 by multiple serine/threonine (Ser/Thr) kinases. Upon phosphorylation, CREB binds the transcriptional co-activator, CBP (CREB-binding protein), to initiate CREB-dependent gene transcription.

    CREB is a critical regulator of cell differentiation, proliferation and survival in the nervous system. Recent studies have shown that CREB is involved tumor initiation, progression and metastasis, supporting its role as a proto-oncogene. Overexpression and overactivation of CREB were observed in cancer tissues from patients with prostate cancer, breast cancer, non-small-cell lung cancer and acute leukemia while

    down-regulation of CREB in several distinct cancer cell lines resulted in inhibition of cell proliferation and induction of apoptosis, suggesting that CREB may be a promising target for cancer therapy. Although CREB, as a transcription factor, is a challenging target for small molecules, various small molecules have been discovered to inhibit CREB phosphorylation, CREB-DNA, or CREB-CBP interaction. These results suggest that CREB is a suitable transcription factor for drug targeting and therefore targeting CREB could represent a novel strategy for cancer therapy.
     

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