1.Phosphoenolpyruvate-dependent phosphotransferase system of Staphylococcus aureus: factor IIIlac, a trimeric phospho-carrier protein that also acts as a phase transfer catalyst.
Deutscher J;Beyreuther K;Sobek HM;Stüber K;Hengstenberg W Biochemistry. 1982 Sep 28;21(20):4867-73.
Factor IIIlac (FIII) consists of three identical subunits. It could be shown that each of the subunits carries a phosphoryl group upon phosphorylation (P-FIII) with phosphoenolpyruvate (PEP), enzyme I, and histidine-containing phospho-carrier protein (HPr). The phosphoryl group is bound to a histidyl residue in P-FIII. Each subunit of FIII contains four histidyl residues. After tryptic cleavage a peptide was isolated that contained one other histidyl residue besides the active center histidine. By further cleavage of the peptide T-2 with V-8 Staphylococcus aureus protease it could be shown that His-19 in the sequence of the peptide T-2 is the active center histidine. Another peptide (1-38), caused by incomplete tryptic cleavage, could be isolated. It inhibited the phospho-transfer reaction from PEP to the sugar molecule at the step of factor III-enzyme II recognition. It competes with factor III for the binding site of enzyme II, the membrane component. It is a very hydrophobic peptide. This hydrophobic region is buried in factor III. But upon phosphorylation of factor III it is turned out. Thus P-FIII binds to Triton X-100 micelles whereas factor III does not. This conformational change caused by phosphorylation could be shown by proton nuclear magnetic resonance methods [Kalbitzer, H.
2.Randomized double-blind placebo-controlled trial of peptide T for HIV-associated cognitive impairment.
Heseltine PN;Goodkin K;Atkinson JH;Vitiello B;Rochon J;Heaton RK;Eaton EM;Wilkie FL;Sobel E;Brown SJ;Feaster D;Schneider L;Goldschmidts WL;Stover ES Arch Neurol. 1998 Jan;55(1):41-51.
BACKGROUND: ;Cognitive impairment is a common consequence of human immunodeficiency virus (HIV) infection, and dementia is one of the diseases that defines the acquired immunodeficiency syndrome. Peptide T (d-ala-peptide-T-amide) has been reported to block the binding of gp120 to brain tissue and to protect neurons from the toxic effects of gp120 in vitro. In pilot studies, administration of peptide T to HIV-positive patients with cognitive impairment was associated with improvement in cognition and constitutional symptoms.;OBJECTIVE: ;To determine whether the intranasal administration of peptide T would improve cognitive function of HIV-positive patients with cognitive impairment.;PATIENTS AND METHODS: ;This was a 3-site, double-blind, placebo-controlled trial of peptide T given intranasally at a dosage of 2 mg 3 times a day for 6 months. Participants were HIV-seropositive persons with evidence of cognitive deficits on a screening test battery. Concomitant antiretroviral therapy was allowed. Randomization to the 2 study arms was balanced according to several stratification variables, such as CD4+ cell count, severity of cognitive impairment, and antiretroviral therapy at study entry.
3.A 500 MHz study of peptide T in a DMSO solution.
Picone D;Temussi PA;Marastoni M;Tomatis R;Motta A FEBS Lett. 1988 Apr 11;231(1):159-63.
Peptide T, an octapeptide of sequence ASTTTNYT that binds to human T cells, was studied as a zwitterion in DMSOd6 solution by means of proton NMR spectroscopy at 500 MHz. The unusual dispersion of the resonances of residues of the same type (T) makes it possible to assign all resonances to specific residues by means of several 2D techniques. The non-random nature of the conformation is substantiated by the observation of sequential nuclear Overhauser enhancements (NOEs). The low value of the temperature coefficient of the chemical shift of the NH of T8 and a diagnostic NOE between the NHs of T7 and T8 hint that a beta-turn including T5, N6, Y7 and T8 is a prominent conformational feature in solution. The ring current high field shifts of the methyl group and of the NH of T8 are consistent with an interaction with the side-chain of Y7, favoured by the beta-turn.