Disease relevance of CD3G

• Several non-random translocation breakpoints associated with leukemia or lymphoma have been shown to occur in chromosome band 11q23 between the genes CD3G and PBGD, a distance of approximately 750 kb [1].
• The molecular basis of the tissue-specific regulation of expression of the human CD3G and D genes were examined using DNase I hypersensitivity and CpG methylation analysis [2].

High impact information on CD3G

• We recently showed that breakpoints in four 11q23 translocations, t(4;11)(q21;q23), t(6;11)(q27;q23), t(9;11)(p22;q23), and t(11;19)(q23;p13.3), were contained within a yeast artificial chromosome clone bearing the CD3D and CD3G gene loci [3].
• Furthermore, we show that a second 11q23 breakpoint, t(11;14)(q23;q32), which was also previously mapped between CD3G and PBGD, is distinct from that of the t(4;11) chromosome [1].
• A combination of yeast artificial chromosome (YAC) cloning, in situ hybridization, and pulsed field gel electrophoresis (PFGE) experiments has further refined the interval containing one of these breakpoints, t(4;11)(q21;q23), to within 200 kb of CD3G [1].
• A rearrangement of the CD3G gene has been observed in a cell line derived from a patient with the t(4;11) translocation and in a hybrid cell line containing the derivative 11q chromosome derived from this cell line, using the restriction enzymes SacII and ClaI [4].
• Thus, we are able to localize such breakpoints, and consequently any affected candidate genes, to the 750 kb between CD3G and PBGD [5].

Biological context of CD3G

• Hybridization of genomic DNA from a yeast clone containing yeast artificial chromosomes (YACs), that carry 320 kilobases (kb) of human DNA including CD3D and CD3G genes, showed that the YACs were split in all four translocations [6].
• The distinct phenotype of CD3G deficiency sheds light on the differential roles of CD3 subunits in T-lymphocyte development [7].
• The transmembrane orientation of the TcR chains and of CD 3 gamma and CD 3 delta can be directly inferred from their primary structure, based on the presence of concensus N-linked glycosylation sites N-terminal of their transmembrane domains [8].
• 3,5,3'-Triiodothyronine (T3) clearance and T3-glucuronide (T3G) appearance kinetics in plasma of freshwater-reared male tilapia, Oreochromis mossambicus [9].
• In the 5 times diluted faecal suspensions of GF and ID rats up to 15% hydrolysis of T3G was still observed [10].

Anatomical context of CD3G

• These results contrast with the partial T-cell immunodeficiency caused by a deficiency in CD3G [7].
• We here show that, compared to fibroblasts from other anatomical locations, the capacity of cardiofibroblasts to secrete T4G and T3G is highest [11].
• H9c2(2-1) myotubes, a model system for cardiomyocytes, take up T4G and T3G at a rate that is 10-15 times higher than that for the unconjugated thyroid hormones [11].
• It may involve conjugation to the glucuronide forms (T4G and T3G) in the mucosal cell with subsequent deconjugation prior to appearance in the portal vein blood [12].

Associations of CD3G with chemical compounds

• Rat cardiac fibroblasts produce and secrete glucuronidated thyroxine (T4G) and 3,3',5-triiodothyronine (T3G) [11].
• This might have physiological significance for the tilapia, with T3G providing a reversible storage form of T3 in blood, as has been suggested for sulfate conjugates of T3 and T4 in blood of several mammals [9].

References