The physiological role of the colony forming units-spleen (CFU-S) inhibitor Acetyl-N-Ser-Asp-Lys-Pro (AcSDKP) has been studied by observing the effects of AcSDKP deprivation. This deprivation was obtained by injecting polyclonal antiserum directed against AcSDKP into normal untreated mice in order to neutralize the endogenous inhibitor. The dramatic increase in the percentage of CFU-S in DNA synthesis as compared to controls receiving anti-KLH antiserum suggests that AcSDKP plays an important role in the maintenance of CFU-S in physiological quiescent state.
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