Chetomin is a natural metabolite produced by several species of the genus Chaetomium. Chetomin disrupts the hypoxia-inducible factor (HIF) pathway, blockomg the interaction of HIF1α and HIF2α with transcriptional co-activators p300 and cAMP response element binding (CREB) binding protein (CBP), thereby attenuating hypoxia-inducible transcription. Disrupting the ability of tumors to adapt to hypoxia leads to decreased tumor growth; hypoxia can also promote resistance to radiotherapeutics. By both of these mechanisms, chetomin shows promise as a lead compound in antitumor research. Chetomin also suppresses the proliferation of LPS-induced mouse spleen lymphocytes.
Chetomin is a natural metabolite produced by several species of the genus Chaetomium. Chetomin is an epidithiodioxopiperazine known to disrupt the hypoxia-inducible factor (HIF) pathway. Chetomin blocks the interaction of HIF1α and HIF2α with transcriptional co-activators p300 and cAMP response element binding (CREB) binding protein (CBP), thereby attenuating hypoxia-inducible transcription. Disrupting the ability of tumors to adapt to hypoxia leads to decreased tumor growth and can serve as an antitumor stratagy. Chetomin also suppresses the proliferation of LPS-induced mouse spleen lymphocytes.
Chetomin is a natural metabolite, which blocks the interaction of HIF1α and HIF2α with transcriptional co-activators p300 and cAMP response element binding (CREB) binding protein (CBP), thereby attenuating hypoxia-inducible transcription. Chetomin also suppresses the proliferation of LPS-induced mouse spleen lymphocytes.
Endothelin-1 (ET-1) is mainly secreted by endothelial cells and acts as a potent vasoconstrictor. In addition ET-1 has also been shown to have pleiotropic effects on a variety of other systems including adaptive immunity. There are two main ET-1 receptors
Aberrant differentiation is a characteristic feature of neoplastic transformation, while hypoxia in solid tumors is believed to be linked to aggressive behavior and poor prognosis. However, the possible relationship between hypoxia and differentiation in malignancies remains poorly defined. Here we
Journal of cellular physiology, 223(2), 359-368 (2010-01-30)
Survival strategies adopted by tumor cells in response to a hypoxic stress include activation of hypoxia-inducible factor 1 (HIF-1) and autophagy. However, the importance and the function of each molecular response is not well defined. In the present study, we
Hypoxia-inducible factor-1 (HIF-1) overexpression has been linked to tumor progression and poor prognosis. We investigated whether targeting of HIF-1 using chetomin, a disrupter of the interaction of HIF-1 with the transcriptional coactivator p300, influences the radiosensitivity of hypoxic HT 1080
A series of epipolythiodioxopiperazines in the fungus Chaetomium cochliodes was investigated using reversed-phase liquid chromatography with diode array detection and electrospray quadrupole time-of-flight-type tandem mass spectrometry in the positive ion mode. The fragmentation of protonated molecular ions including low-abundance parent
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