Unlabelled: The functional organization of the primary visual area (V1) and the importance of sensory experience in its normal development have been well documented in eutherian mammals. However, very few studies have investigated the response properties of V1 neurons in another large class of mammals, or whether sensory experience plays a role in shaping their response properties. Thus we reared opossums (Monodelphis domestica) in normal and vertically striped cages until they reached adulthood.
View Article and Find Full Text PDFDefinition of cell cycle control proteins that modify tumor cell resistance to estrogen (E2) signaling antagonists could inform clinical choice for estrogen receptor positive (ER+) breast cancer (BC) therapy. Cyclin G2 (CycG2) is upregulated during cell cycle arrest responses to cellular stresses and growth inhibitory signals and its gene, CCNG2, is directly repressed by E2-bound ER complexes. Our previous studies showed that blockade of HER2, PI3K and mTOR signaling upregulates CycG2 expression in HER2+ BC cells, and that CycG2 overexpression induces cell cycle arrest.
View Article and Find Full Text PDFLearning and memory as well as long-term potentiation (LTP) depend on Ca (2+) influx through the NMDA-type glutamate receptor (NMDAR) and the resulting activation of the Ca (2+) and calmodulin-dependent protein kinase (CaMKII). Ca (2+) influx via the NMDAR triggers CaMKII binding to the NMDAR for enhanced CaMKII accumulation at post-synaptic sites that experience heightened activity as occurring during LTP. Previously, we generated knock-in (KI) mice in which we replaced two residues in the NMDAR GluN2B subunit to impair CaMKII binding to GluN2B.
View Article and Find Full Text PDFTo maintain genomic integrity DNA damage response (DDR), signaling pathways have evolved that restrict cellular replication and allow time for DNA repair. CCNG2 encodes an unconventional cyclin homolog, cyclin G2 (CycG2), linked to growth inhibition. Its expression is repressed by mitogens but up-regulated during cell cycle arrest responses to anti-proliferative signals.
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