Are h3K9me3-binding proteins dispensable for SETDB1/H3K9me3-dependent retroviral silencing?
Taken together, these results reveal that each of the known H3K9me3-binding proteins is dispensable for SETDB1-mediated ERV silencing. We speculate that H3K9me3 might maintain ERVs in a silent state in mESCs by directly inhibiting deposition of active covalent histone marks.
Extensive literature supports the view that upregulated arginase activity in cavernosal tissue can reduce NOS function and NO production. Excessive arginase activity has been shown to contribute to the progression of aging-, hypertension- and diabetes-induced vascular dysfunction as well as ED. Earlier studies have shown that RhoA/ROCK and subsequent activation of p38 MAPK mediate elevation of arginase expression/activity in diabetic and hypertensive mice. Reducing corporal arginase activity by gene-based or pharmacological therapy and/or inhibition of upstream regulators of arginase expression may provide novel therapeutic approaches in the management of ED.