Translocation and stability of replicative DNA helicases upon encountering DNA-protein cross-links.

DNA-protein cross-links (DPCs) are formed when cells are exposed to various DNA-damaging agents. Because DPCs are extremely large, steric hindrance conferred by DPCs is likely to affect many aspects of DNA transactions. In DNA replication, DPCs are first encountered by the replicative helicase that moves at the head of the replisome.

Repair and biochemical effects of DNA-protein crosslinks.

Genomic DNA is associated with various structural, regulatory, and transaction proteins. The dynamic and reversible association between proteins and DNA ensures the accurate expression and propagation of genetic information. However, various endogenous, environmental, and chemotherapeutic agents induce DNA-protein crosslinks (DPCs), and hence covalently trap proteins on DNA.

Functional interaction of regulator of G protein signaling-2 with melanin-concentrating hormone receptor 1.

Melanin-concentrating hormone receptor 1 (MCHR1) is a G protein-coupled receptor (GPCR) highly expressed in the central nervous system. MCHR1 mediates many physiological functions including energy homeostasis and emotional processing. By acting as GTPase-activating proteins, regulators of G protein-signaling (RGS) proteins are negative modulators of GPCRs.

Regulation of melanin-concentrating hormone receptor 1 signaling by RGS8 with the receptor third intracellular loop.

Melanin-concentrating hormone (MCH) receptor 1 (MCH1R) belongs to the class A G protein-coupled receptors (GPCRs). The MCH-MCH1R system plays a central role in energy metabolism, and thus the regulation of signaling pathways activated by this receptor is of particular interest. Regulator of G protein signaling (RGS) proteins work by increasing the GTPase activity of G protein alpha subunits and attenuate cellular responses coupled with G proteins.