Rotem Karni

TL;DR: It is found that the splicing factor SF2/ASF is upregulated in various human tumors, in part due to amplification of its gene, SFRS1, and can act as an oncoprotein and is a potential target for cancer therapy.

TL;DR: SRSF 1 can promote breast cancer, and SRSF1 itself or its downstream effectors may be valuable targets for the development of therapeutics.

TL;DR: Intracellularly, genetic and pharmacologic manipulations reveal that glucose induces β cell replication via metabolism by glucokinase, the first step of glycolysis, followed by closure of K(ATP) channels and membrane depolarization, providing a molecular mechanism for homeostatic control of β cell mass by metabolic demand.

TL;DR: The induced expression of c-SRC antisense RNA or the application of a selective Src kinase inhibitor induces growth arrest, programmed cell death and reverses the transformed properties of cells that overexpress EGFR or HER-2 receptors, suggesting that Src positively regulates Bcl-XL expression via Stat3 activation and thus acts not only as a potent mitogenic signaling element, but also as an anti-apoptotic signaling protein.

TL;DR: The results reveal a mechanism by which lncRNA MALAT1 acts as a proto-oncogene in hepatocellular carcinoma, modulating oncogenic alternative splicing through SRSF1 upregulation.