Disease relevance of Skull26

• E19 blocked the presentation of vaccinia and influenza virus proteins to CTLs in a MHC class I allele-specific manner identical to its inhibition of MHC class I transport from the endoplasmic reticulum [1].
• Retention of adenovirus E19 glycoprotein in the endoplasmic reticulum is essential to its ability to block antigen presentation [2].
• Three murine monoclonal antibodies (MAb), E19, E205, and E251, raised against pertussis toxin reacted in Western blots (immunoblots) with the S1, S4, and S2-S3 subunits, respectively, and neutralized the Chinese hamster ovary cell-clustering activity of pertussis toxin [3].
• The earliest immunoreactivity was found at E17 in vestibular hair cells (VHCs), then, at E19, in afferent fibers entering the sensory epithelia and in rare ganglion neurons [4].
• Sheets of E19 rat retina with or without retinal pigment epithelium (RPE) were transplanted to the subretinal space in 33 Royal College of Surgeons (RCS) and transgenic s334ter-5 rats with retinal degeneration [5].

High impact information on Skull26

• The role of exocytosis of major histocompatibility complex (MHC) class I molecules in the presentation of antigens to mouse cytotoxic T lymphocytes (CTLs) was examined by use of a recombinant vaccinia virus that expresses the E19 glycoprotein from adenovirus [1].
• Unlike E3/19K, however, delta E19 was transported through the Golgi complex to the plasma membrane, where it could be detected biochemically and immunocytochemically using a monoclonal antibody specific for the lumenal domain of E3/19K [2].
• In WT E19 skeletal and cardiac muscles, Fxr1p is localized to the costameric regions within the muscles [6].
• Both proteins are widely expressed and developmentally regulated with expression peaking at E19 in mouse spinal cord. hnRNP-R binds RNA through its RNA recognition motif domains [7].
• RT-PCR on mouse tissues showed expression in the thymus, stomach, testis and E19 embryos [8].

Biological context of Skull26

• Hybrid class I molecules, in which exons encoding domains of A2.1 and H-2Dd had been exchanged, were used to define the regions of A2.1 required for E19 association [9].
• To ascertain the role of CD8(+) T cell-induced beta cell lysis in the initiation of diabetes, we expressed a rat insulin promoter (RIP)-driven adenovirus E19 transgene in NOD mice [10].
• Of further interest, the mouse SULT2B1 and SULT2A1 genes are differentially expressed during embryonic development, with the former being expressed at all stages from E8.5-E19, whereas the latter is not expressed until E19 [11].
• Pregnant mice were exposed to a gamma source at 16, 17, and 19 days of gestation (E16, E17, and E19, respectively), with total doses of 2 Gy and 3 Gy, in order to produce brain defects on their progeny [12].
• Intraocular pertussis toxin administered at E13 increased cell death of isthmo-optic neurons by 42%, whereas injections at E19 had no effect [13].

Anatomical context of Skull26

• Histochemical analyses carried out on both skeletal and cardiac muscles show a disruption of cellular architecture and structure in E19 Fxr1 neonates compared with wild-type (WT) littermates [6].
• This correlates with the almost complete degeneration of the müllerian ducts in male embryos at E19 [14].
• Serial paraffin sections of E17 and E19 fetuses were examined for histologic evidence of inflammation [15].
• In situ hybridization of skin from E18, E19, and 4-day-old neonatal rats demonstrates that interfollicular and follicular keratinocytes express KPRP [16].
• Expression of Caspase and Bcl-2 proteins was examined in the hippocampus of senescence-accelerated mice (SAM, P8 and R1 strain) from E19 to 16 months of age [17].

Associations of Skull26 with chemical compounds

• We labeled cells generated on E18 and E19 and the day of birth (P0) with bromodeoxyuridine and followed their fates over the following 20 days [18].
• Similar percentages of both E17 and E19 donor-derived neurons expressed neurotransmitters and receptors [glutamate, aspartate, GABA, GABA receptor (GABA-R), NMDA-R, AMPA-R, and kainate-R] appropriate for endogenous adult CPNs progressively over a period of 2-12 weeks after transplantation [19].

Analytical, diagnostic and therapeutic context of Skull26

• Mouse embryos from day 13 to day 19 of gestation (E13 through E19) were removed by Caesarean section and their brains were prepared for electron microscopy [20].
• Fluorescent beads (1 micron, diameter), injected into the amniotic fluid surrounding E18 mouse fetuses, were sought in serial frozen sections of E19 animals [21].
• Immunoblotting and apoptosis assay were performed to study the relationship between the decreased expression of Bcl-2 and neuronal death on the brains of Gaucher mice fetuses at embryonic day 17.5 (E17.5) and E19 [22].
• Retrograde labeling with FluoroGold revealed that 42 +/- 2% of transplanted E19 immature S1 neurons formed connections with the contralateral S1 cortex by 12 weeks after transplantation, compared with 23 +/- 7% of E17 neurons [19].

References