Disease relevance of TRIM39

• Three human immunodeficiency virus protease cleavage sites within gag (p2/NC, NC/p1, and NC/TFP) showed considerable in vivo evolution before and after therapy with indinavir, ritonavir, and/or saquinavir [1].

High impact information on TRIM39

• In marked contrast with this, with P-Tyr99-calmodulin there were 3-4-fold increases in the IC50 values for inhibition of type-I PDE activity by the calmodulin antagonists TFP and W7, together with increased values for Hill coefficients for inhibition [2].
• Analyses of glucosinolate hydrolysis products in L. sativum autolysates and TFP transcript accumulation revealed an organ-specific regulation of thiocyanate formation [3].
• TFP does not only catalyze thiocyanate and simple nitrile formation from benzylglucosinolate but also the formation of simple nitriles and epithionitriles from aliphatic glucosinolates [3].
• We investigated glucosinolate hydrolysis in Lepidium sativum and identified a thiocyanate-forming protein (TFP) that shares 63-68% amino acid sequence identity with known ESPs and up to 55% identity with myrosinase-binding proteins from Arabidopsis thaliana, but differs from ESPs in its biochemistry [3].
• KN-62, a specific inhibitor of calmodulin-dependent protein kinase II acted on the monolayer like PIM, whereas ML-7, a specific inhibitor of myosin regulatory light chain kinase, inhibited lymphoid cell motility like TFP and CP [4].

Biological context of TRIM39

• The results not only confirmed that the p-arm of domestic cat B2 is inverted relative to human Chromosome 6, but also demonstrated that one inversion breakpoint localized to the distal segment of the MHC class I between TRIM39 and TRIM26 [5].
• The inversion thus disjoined the approximately 2.85 Mb of MHC containing class II-class III-class I (proximal region) from the approximately 0.50 Mb of MHC class I/extended class I region, such that TRIM39 is adjacent to the Chromosome B2 centromere and TRIM26 is adjacent to the B2 telomere in the domestic cat [5].
• The identification of TFP defines a new family of proteins that control glucosinolate hydrolysis and challenges the previously proposed reaction mechanism of epithionitrile formation [3].
• It was found that DNA alkylation at the N-7 guanine with the bulky alkylating reagent, N,N,N'-tri-(beta-chloroethyl)-N'-(p-formylphenyl)propylene diamine-1,3 (TFP) is much diminished when DNA is double-stranded [6].
• DNA-PKcs and Ku86 cleavage were evident in U-1810 cells after 30 min incubation with 100 microM TFP, along with changes in the cells consistent with apoptosis [7].

Anatomical context of TRIM39

• We assessed the effect of trifluoperazine and chlorpromazine (TFP and CP, two strong inhibitors of lymphocyte motility) and pimozide (PIM, a much weaker inhibitor of lymphocyte motility but a strong inhibitor of calmodulin) on invasion of human Molt-4 T-cells across precultured fibroblast monolayers [4].
• CONCLUSION: Medium supplementation with the growth factor combination TFP during chondrocyte expansion supports higher proliferation rates at any age and higher post-expansion chondrogenic capacity in donors up to 40 years [8].

Associations of TRIM39 with chemical compounds

• The A23187 induced calcium uptake in ATP depleted cells was determined at pH 6.9 in the presence of trifluoperazine (TFP, 0.30 mM), compound 48/80 (0.89 mg/ml), 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8, 2.13 mM) and verapamil (1.81 mM) [9].
• Guanines in the hairpin formed by palindrome of 9 bp were protected from TFP action, while dimethyl sulfate modified all guanines [6].
• 5'-Labeled ss fragment was modified with TFP and cleaved by piperidine hydrolysis at the alkylated guanine residues according to the Maxam-Gilbert procedure [6].

Analytical, diagnostic and therapeutic context of TRIM39

• Chondrogenic capacity of CTR- and TFP-expanded cells was assessed by cultivation as 3D pellets in a defined serum-free medium, followed by histological, immunohistochemical, biochemical and real-time RT-PCR analyses [8].

References