DiscoveryProbe™ Endocrinology and Hormones-related Compounds Panel
A wide range of well-characterized bioactive molecules that covers various targets related to endocrinology and hormones, including androgen receptor, estrogen/progestogen receptor and RAAS etc. Facilitate your research towards the insights of diabetes, thyroid disorders and cancer etc. Applicable in cellular assays, animal models and drug screenings etc.
Related Biological Data
KLK3 (top) and NKX3-1(bottom) expression which were the AR target genes in various resistant clones were analyzed by QPCR. All lines were pretreated with vehicle (−) or doxycycline (+) for 3 days before treatment with DMSO (left) or 10 μmol/L MDV3100 (right) for 24 hours in 10% FCS. TBP was used to normalize expression. Data represent mean ± SEM; n = 3. *, P < 0.05; **, P < 0.01 (Student t test). The F876L mutation is sufﬁcient to induce genetic and phenotypic resistance to MDV3100.
Review (Georgia Regents University)
Comparison of different anti-androgen/AR compounds on TGF-β1/Smad3/MMP9 signaling in PCa cells. CWR22Rv1 cells treated with 10 μM CASO, 10 μM MDV, 10 μM ASC, 5 μM CTS, or vehicle for 3 days were harvested. The expressions of TGF-β1, p-Smad3, Smad3, MMP9, and GAPDH were analyzed by Western blot analysis. All of the experiments have been repeated twice independently. *, p< 0.05; **, p < 0.01; ***, p < 0.001. Error bars, S.D. Casodex and MDV3100 enhanced TGF-beta, MMP9 expression in CWR22Rv1 cells. whereas ASC-J9 and CTS treatment did not.
Review (University of Glasgow )
Chronic exposure to ENZA resulted in autophagy. To mimic resistant to ENZA, C4-2B cells were subjected to 20 μM ENZA over a period of 3 months and selected for a sub-population of resistance cells (C4-2B+R). Upper panel showed acridine orange staining of autophagosome acidic vesicles as a marker for autophagy. Lower panel showed LC3-I/II protein expression in parental cells (control) and under chronic ENZA exposure-treated vehicle control, chloroquine (CQ) or CMI. β -Actin was used as the loading control.