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Abstract Most characterized anti-CRISPR proteins act via well-defined core inhibitory mechanisms, yet how auxiliary structural elements modulate and potentiate these canonical processes remains poorly understood. Here, we show that AcrIIC1Boe represses Nme1Cas9 activity through an integrated, loop-coupled regulatory mode.
As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
