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This could occur through mechanisms such as altering the formation or function of immune synapses

Genes that were consistently differentially expressed when UQCR-C1 was knocked down were of a particular interest since those represent a core set of genes responding to UQCR-C1 silencing, regardless of the infection status or timepoint

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(2006), who demonstrated that BPC-157 improved the quality and rate of tendon-to-bone reattachment in a rat detached supraspinatus model, with histological evidence of improved collagen organization at the repair interface (Krivic et al., 2006, Journal of Orthopaedic Research