nucleus translocation

4-Hydroxytamoxifen (ICI 79280) is the active metabolite of Tamoxifen, an estrogen receptor modulator (SERM) with selective and oral potency. 4-Hydroxytamoxifen has antitumor activity and may be used in breast cancer research.

Asperbisabolane L, a sesquiterpenoid, exhibits anti-inflammatory effects through the inhibition of the NF-κB-activated pathway. It prevents the translocation of NF-κB from the cytoplasm to the nucleus and also reduces NO production in LPS-activated BV-2 microglia cells.

DC271, a retinoid and RAR agonist, mimics the cellular effects of the endogenous ATRA and the synthetic EC23, by binding to retinoid protein machinery such as CRABPII to facilitate the translocation of ATRA into the nucleus [1].

Aeruginosin 865, a compound extracted from the terrestrial cyanobacterium Nostoc sp. Luke ová 30/93, represents the inaugural aeruginosin-type peptide to incorporate a fatty acid and a carbohydrate moiety. It functions by inhibiting the translocation of NF-kB to the nucleus, thereby exerting an anti-inflammatory effect.

Octahydrocurcumin has antioxidant and and anti-inflammatory activities, it can inhibit the lipopolysaccharide (LPS)-induced inflammatory response via the mechanism of inhibiting NF-kB translocation to the nucleus. Octahydrocurcumin exhibits potent cytotoxic effect (IC50 =19.46 ug/mL) and shows high antimicrobial activity.

TSPA is an ATF6α translocation inducer which effectively promotes ATF6α translocation into the nucleus and ameliorates glucose homeostasis on db/db mice.

TTC-352 is an orally bioavailable selective human estrogen receptor alpha (ERalpha; ESR1; ERa) partial agonist (ShERPA), with potential antineoplastic activity. Upon administration, TTC-352 mimics the naturally-occurring 17beta-estradiol (E2) and targets and binds to ERa located in the nucleus. This causes translocation of ERa to extranuclear sites. Nuclear export of ERa prevents normal ER-mediated signaling and inhibits proliferation of ER-positive tumor cells.

MPT0B098 is a potent microtubule inhibitor through binding to the colchicine-binding site of tubulin. MPT0B098 is active against the growth of various human cancer cells, including chemoresistant cells with IC50 values ranging from 70 to 150 nmol/L. MPT0B098 arrests cells in the G2–M phase and subsequently induces cell apoptosis. In addition, MPT0B098 effectively suppresses VEGF-induced cell migration and capillary-like tube formation of HUVECs. Distinguished from other microtubule inhibitors, MPT0B098 not only inhibited the expression levels of HIF-1α protein but also destabilized HIF-1α mRNA. The mechanism of causing unstable of HIF-1α mRNA by MPT0B098 is through decreasing RNA-binding protein, HuR, translocation from the nucleus to the cytoplasm. Notably, MPT0B098 effectively suppresses tumor growth and microvessel density of tumor specimens in vivo. Taken together, our results provide a novel mechanism of inhibiting HIF-1α of a microtubule inhibitor MPT0B098. MPT0B098 is......

1. 5,7-Dihydroxychromone (5,7-Dihydroxy-4H-Chromen-4-One) isolated from DME is one of the active compounds that may contribute to regulate blood glucose levels. 2. 5,7-Dihydroxychromone exerts neuroprotective effect against 6-OHDA-induced oxidative stress and apoptosis by activating Nrf2/ARE signal . 3. 5,7-Dihydroxychromone induces the translocation of Nrf2 to the nucleus and increases Nrf2/ARE binding activity which results in the up-regulation of the expression of Nrf2-dependent antioxidant genes, including HO-1, NQO1, and GCLc.

Alisol B acetate can induce Bax nuclear translocation and apoptosis in human hormone-resistant prostate cancer PC-3 cells, the Bax activation and translocation from the cytosol to nucleus might be a crucial response to the apoptotic effect. Alisol B aceta

Triamcinolone (Aristocort) is a synthetic glucocorticoid with anti-inflammatory and immunomodulating properties. Upon cell entry, triamcinolone binds to and activates the glucocorticoid receptor, which leads to translocation of the ligand-receptor complex to the nucleus and induces expression of glucocorticoid-responsive genes such as lipocortins. Lipocortins inhibit phospholipase A2, thereby blocking the release of arachidonic acid from membrane phospholipids and preventing the synthesis of prostaglandins and leukotrienes, both mediators of inflammation. In addition, pro-inflammatory cytokine production, including interleukin (IL)-1and IL-6, and the activation of cytotoxic T-lymphocytes is also inhibited. T-cells are prevented from making IL-2 and proliferating. This agent also decreases the number of circulating lymphocytes, induces cell differentiation, and stimulates apoptosis through increasing Ikappa-B expression and curtailing activation of nuclear factor (NF)kappa-B.