ER functions of oncogenes and tumor suppressors: Modulators of intracellular Ca(2+) signaling.
Leuven, Belgium. In Biochim Biophys Acta, Feb 2016
An important aspect of this is the identification of several major oncogenes, including Bcl-2, Bcl-XL, Mcl-1, PKB/Akt, and Ras, and tumor suppressors, such as p53, PTEN, PML, BRCA1, and Beclin 1, as direct and critical regulators of Ca(2+)-transport systems located at the ER membranes, including IP3 receptors and SERCA Ca(2+) pumps.
Lipid droplets go nuclear.
Cambridge, United States. In J Cell Biol, Feb 2016
show that the nuclear membrane, promyelocytic leukemia bodies, and the protein PML-II play a role in nuclear LD formation, suggesting functional relationships between these structures.
Synthetic lethal targeting of oncogenic transcription factors in acute leukemia by PARP inhibitors.
Hong Kong, Hong Kong. In Nat Med, Dec 2015
Here we demonstrate that AML driven by repressive transcription factors, including AML1-ETO (encoded by the fusion oncogene RUNX1-RUNX1T1) and PML-RARα fusion oncoproteins (encoded by PML-RARA) are extremely sensitive to poly (ADP-ribose) polymerase (PARP) inhibition, in part owing to their suppressed expression of key homologous recombination (HR)-associated genes and their compromised DNA-damage response (DDR).
[Significance of PLSCR1 in Matrine Induced Differentiation of ATRA Resistant APL Cells].
In Zhongguo Zhong Xi Yi Jie He Za Zhi, Nov 2015
OBJECTIVE: To observe the expression of phospholipid scramblase 1 (PLSCR1) in matrine (MAT) induced differentiation of all-trans retinoic acid (ATRA) resistant acute promyelocytic leukemia (APL) cells, and to explore its correlation to cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signal pathway.
Active Pin1 is a key target of all-trans retinoic acid in acute promyelocytic leukemia and breast cancer.
More papers using
Boston, United States. In Nat Med, May 2015
By using mechanism-based screening, here we find that all-trans retinoic acid (ATRA)--a therapy for acute promyelocytic leukemia (APL) that is considered the first example of targeted therapy in cancer, but whose drug target remains elusive--inhibits and degrades active Pin1 selectively in cancer cells by directly binding to the substrate phosphate- and proline-binding pockets in the Pin1 active site.