Disease relevance of Tcrb

• However, cytocidal toxicity of 2-FAA was substantially potentiated by either 3-methylcholanthrene [(MCA) CAS: 56-49-5] or 3,3',4,4'-tetrachlorobiphenyl [(TCBP) CAS: 32598-13-3], an MCA-type PCB [1].
• Authentic OGP is identical to the C-terminus of histone H4 and shares a five residue motif with a T-cell receptor beta-chain V-region and the Bacillus subtilis outB locus [2].
• T cells with similar T-cell receptor beta-chain complementarity-determining region 3 motifs infiltrate inflammatory lesions of synthetic peptides inducing rat autoimmune myocarditis [3].
• A single cysteinyl adduct, inferred to be 5-cysteinyl-3, 6-dichloro-4-(2',5'-dichlorophenyl)-1,2-benzoquinone, was detected in brain cytosolic protein of rats treated with multiple doses of TCB with levels of 15.2 (pmol/g)/(mg/kg of body weight) [4].
• The autoreactive T cell population in experimental allergic encephalomyelitis: T cell receptor beta-chain rearrangements [5].

High impact information on Tcrb

• CDR1 T-cell receptor beta-chain peptide induces major histocompatibility complex class II-restricted T-T cell interactions [6].
• Since this cell type is also known to influence T-cell receptor expression in developing thymocytes, we examined the thymic and peripheral T-cell receptor beta chain variable region repertoire in diabetes-prone and diabetes-resistant rats [7].
• Organization and nucleotide sequence of the rat T cell receptor beta-chain complex [8].
• Incubation of phenobarbital-induced rat liver microsomes with 2,2',5,5'-tetrachlorobiphenyl (TCB) yielded about 30% of the substrate as 3-hydroxy-TCB, 3,4-dihydroxy-TCB, 3,3'-dihydroxy-TCB (tentative identification), and 3,4-dihydro-3,4-dihydroxy-TCB in relative amounts of about 1:1:0.05:0.05 [9].
• Under identical conditions, 2,2',5,5'-tetrachlorobiphenyl 3,4-oxide (TCBO) yielded about 45% of the substrate as the above products in an approximate ratio of 0.1:1:0.01:1, as well as 10% as TCB [9].

Chemical compound and disease context of Tcrb

• This increase in TCBP provided no protection against cadmium toxicity in the testes [10].
• Trans-1,2-diphenylcyclobutane (TCB), cis-1,2-diphenylcyclobutane (CCB), 1,3-diphenylpropane, 2,4-diphenyl-1-butene, 2,4,6-triphenyl-1-hexene, and 1-alpha-phenyl-4ss-(1 -phenylethyl)tetralin were negative in the yeast estrogen screening assay and estrogen reporter assay using estrogen-responsive human breast cancer cell line MCF-7 [11].
• The increase in 5'D-II activity suggests that local hypothyroidism occurs in the brains of fetal and neonatal rats exposed to HCB and/or TCB [12].
• Measurement of 7-ethoxycoumarin O-deethylase and benzphetamine N-demethylase activities indicated that the loss of protection by HCB or TCB against benzene toxicity after 7 days was not associated with changes in the activities of hepatic mixed-function oxidases inducible by 3-methylcholanthrene or phenobarbital [13].

Biological context of Tcrb

• The Cb1 alleles are one part of larger Tcrb haplotypes, containing V beta, D beta, and J beta elements; complete Cb1 genomic nucleotide sequences, and a partial list of the strain distribution of the two alleles, are described in this report [14].
• Different rat Tcrb haplotypes express either TCR beta variable segment (Tcrb-V) 8.2l or 8.4a [15].
• The results indicate that TCB uncouples the catalytic cycle of CYP1A, ostensibly CYP1A1, resulting in formation of ROS within the active site [16].
• CCB, 1,3-diphenylpropane, and 2,4-diphenyl-1-butene also exhibited estrogenic activity after metabolic activation by liver microsomes, but the activity was lower than that of TCB [11].
• Histopathological analysis confirmed that 98% of the tumours were mammary carcinomas, predominantly in situ ductal carcinomas, but, in addition, revealed that 13 of the tumours had an invasive phenotype of which 12/13 had all arisen in TCB-treated animals [17].

Anatomical context of Tcrb

• Neuritogenic Lewis rat T cells use Tcrb chains that include a new Tcrb-V8 family member [18].
• The formation of 3-hydroxy-TCB and TCBO from TCB via different pathways was consistent with the observation that TCB-treated rats excreted 6-fold higher levels of 3-hydroxy-TCB in their feces than did TCBO-treated rats [9].
• The results suggest that altered growth control is due to a direct effect of TCB on hepatocytes [19].
• In contrast, TCBP microsomes produced predominantly the 5,6-dihydrodiol followed by the 8,9-dihydrodiol, whereas the formation of the 10,11-dihydrodiol is suppressed [20].
• TCB treatment in vivo enhanced EGF-stimulated autophosphorylation of the EGF receptor in liver plasma membranes [19].

Associations of Tcrb with chemical compounds

• Omission of NADPH from incubations of TCBO decreased the yields of 3-hydroxy-TCB, both dihydroxy-TCBs, and TCB by 75-100%, increased the yield of 3,4-dihydro-3,4-dihydroxy-TCB 4-fold, and permitted the recovery of small amounts (0.5% yield) of 4-hydroxy-TCB [9].
• Alterations of hepatocyte growth control by inducers of drug-metabolizing enzymes were investigated using 3,4,3',4'-tetrachlorobiphenyl (TCB) as the inducing agent [19].
• However, biliary excretion of T4 glucuronide was strongly increased by TCB, resulting in an augmented T4 disappearance from the medium, although initial hepatic uptake of T4 was not altered [21].
• For the determination of a possible interaction of the effects in vivo of 2,5,2',5'-tetrachlorobiphenyl (TCB) and 3,4,3',4'-TCB, rats were exposed to a single dose of diethylnitrosamine (DEN) and subsequently to 0.1 p.p.m. 3,4,3',4'-TCB and/or 10 p.p.m. 2,5,2',5'-TCB in the feed for 1 year [22].
• Treatment with HCB did not increase neonatal ethoxyresorufin-O-de-ethylation (EROD) activities whereas a more than 26-fold increase in EROD activity was noted in response to exposure to TCB [23].

Other interactions of Tcrb

• Diverse T cell receptor beta chain usage by rat encephalitogenic T cells reactive to residues 68-88 of myelin basic protein [24].
• Localization of the rat T-cell receptor beta-chain and carboxypeptidase A1 loci to chromosome 4 [25].

Analytical, diagnostic and therapeutic context of Tcrb

• Adult, female WAG/Rij rats received a single intraperitoneal injection of either vehicle (corn oil), 15 mg TCB/kg, or 200 mg TCB/kg body weight and were sacrificed (N = 3 per group) at 1, 3, 7, and 14 days after treatment [26].
• The exposure of cell cultures to 3,3',4,4'-tetrachlorobiphenyl (TCB) (a non-ortho-subtituted planar congener) does not alter PLA(2) activity [27].
• When TCB was incubated with liver microsomes of phenobarbital-treated rats in the presence of NADPH, three metabolites were detected by high-performance liquid chromatography (HPLC) [11].
• The distribution of radiolabeled 3,4,3',4'-tetrachlorobiphenyl (TCB) and TCB-induced effects on serum and adrenal gland retinoid content, and adrenal gland morphology was studied by liquid scintillation counting, high performance liquid chromatography, light microscopic autoradiography, and transmission electron microscopy [26].
• A single ip dose of 1, 5, or 15 mg/kg 3,4,3',4'-tetrachlorobiphenyl (TCB) caused a dose-dependent depression of plasma retinol levels 24 hr after treatment of female Sprague-Dawley rats [28].

References