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Biomedical subjects

J Bao

Publications and source records attributed to J Bao.

At least 73 records · Page 4Linked to original sources
PubMed1996

Isolation and characterization of Nmi, a novel partner of Myc proteins.

The Myc family of oncogenes is thought to play an important role in cell proliferation, differentiation, and neoplastic transformation. Although the structure and expression of Myc genes are well characterized, the function and biochemical properties of the Myc proteins are less well understood. Here, using a yeast genetic screen, we identified a novel gene, Nmi, that binds to N-myc and C-myc. It also interacts with other transcription factors in yeast. The carboxyl terminus of Nmi shows homology to an interferon-induced leucine zipper protein, IFP 35, whereas its amino terminus is homologous to a coiled-coil heptad repeat in the C. elegans protein, CEF59. Co-precipitation studies of Nmi with N-myc and C-myc confirmed the interaction in mammalian cells. Nmi mRNA is expressed at low levels in all fetal and adult human tissues tested, except brain. Among several cancer cell lines, high expression of Nmi was found in myeloid leukemias, which also express high levels of C-myc. Nmi gene is localized on human chromosome 22q13.3. Translocations of this region have been reported in some human leukemias.

Amino Acid Sequence↗
PubMed1996

Expansion of polyglutamine repeat in huntingtin leads to abnormal protein interactions involving calmodulin.

Huntington's disease (HD) is an inherited neurodegenerative disorder associated with expansion of a CAG repeat in the IT15 gene. The IT15 gene is translated to a protein product termed huntingtin that contains a polyglutamine (polyGln) tract. Recent investigations indicate that the cause of HD is expansion of the polyGln tract. However, the function of huntingtin and how the expanded polyGln tract causes HD is not known. We investigate potential protein-protein interactions of huntingtin using affinity resins. Huntingtin from brain extracts is retained on calmodulin(CAM)-Sepharose in a calcium-dependent fashion. We purify rat huntingtin to apparent homogeneity using a combination of DEAE-cellulose column chromatography, ammonium sulfate precipitation, and preparative SDS/PAGE. Purified rat huntingtin does not interact with CAM directly as revealed by 125I-CAM overlay. Huntingtin forms a large CAM-containing complex of over 1,000 kDa in the presence of calcium, which partially disassociates in the absence of calcium. Furthermore, an increased amount of mutant huntingtin from HD patient brains is retained on CAM-Sepharose compared to normal huntingtin from control patient brains, and the mutant allele is preferentially retained on CAM-Sepharose in the absence of calcium. These results suggest that huntingtin interacts with other proteins including CAM and that the expansion of polyGln alters this interaction.

Animals↗
PubMed1996

Reduced evoked release of acetylcholine in the rodent hippocampus following traumatic brain injury.

The chronic effects of traumatic brain injury on acetylcholine release were evaluated by using in vivo microdialysis. Acetylcholine release was measured in the hippocampus of anesthetized rats 2 weeks after lateral controlled cortical impact (n = 10) or sham surgery (n = 10). Prior to microdialysis, behavioral assessments of motor and spatial memory were performed. Cortical impact (6 meter/s, 2 mm deformation) produced beam balance deficits that persisted for 1 day and beam walking deficits that persisted for 3 days after injury. In addition, spatial memory, as measured by swim latencies in a Morris water maze, was compromised between 10-14 days after injury. Immediately following behavioral testing, the animals were anesthetized with halothane, and a microdialysis probe was placed into the dorsal hippocampus. After a 160 min equilibration period, extracellular levels of acetylcholine were measured prior to and after an intraperitoneal administration of scopolamine (1 mg/kg), which evokes acetylcholine release by blocking autoreceptors. Prior to scopolamine administration, there were no differences in extracellular levels of acetylcholine between injured and sham animals. However, there was a significant reduction of hippocampal acetylcholine release evoked by scopolamine in injured animals as compared to sham controls. In separate control groups, saline administration alone did not change hippocampal acetylcholine release in injured (n = 5) or sham (n = 5) animals. This study represents the first application of in vivo microdialysis to evaluate chronic neurotransmission deficits following TBI. The present study demonstrates that a magnitude of traumatic brain injury (TBI) sufficient to produce spatial memory deficits can result in a reduction in scopolamine-evoked release of acetylcholine within the hippocampus. The data further suggest that presynaptic mechanisms mediating release of acetylcholine could play a significant role in cholinergic neurotransmission deficits following TBI.

Acetylcholine↗
PubMed1996

Diminished microtubule-associated protein 2 (MAP2) immunoreactivity following cortical impact brain injury.

This study employed Western blotting and qualitative immunohistochemistry to analyze the effects of cortical impact traumatic brain injury (TBI) on acute changes in MAP2 immunoreactivity in the rat cortex. We employed a lateral cortical impact injury device to induce severe TBI, which is associated with focal cortical contusion and neuronal death at the impact site. Three hours following TBI, Western blotting detected substantial MAP2 loss only in the cortex ipsilateral to the site of injury. Light microscopic studies of MAP2 revealed a prominent loss of MAP2 immunofluorescence in apical dendrites of pyramidal neurons within layers 3 and 5, as well as a loss of fine dendritic arborization within layer 1. These changes in MAP2 immunolabeling were associated with, but not exclusively restricted to, the presence of dark shrunken neurons labeled by hematoxylin and eosin staining, suggesting impending cell death. Alterations in MAP2 immunofluorescence were found both within and beyond areas of focal contusion and necrosis in the ipsilateral cortex. Thus, traumatic brain injury in rats can produce rapid and significant dendritic pathology within sites of contusion. However, immunohistochemical changes in MAP2 labeling outside of contused regions suggests that TBI-induced dendritic damage may not be exclusively associated with acute cell death.

Animals↗
PubMed1995

Basal and scopolamine-evoked release of hippocampal acetylcholine following traumatic brain injury in rats.

This study employed in vivo microdialysis in awake, freely-moving Sprague-Dawley rats to examine acetylcholine (ACh) release in the dorsal hippocampus at 14 days following lateral controlled cortical impact. Extracellular levels of ACh were measured prior to and after an intraperitoneal administration of scopolamine (1 mg/kg), which evokes ACh release by blocking autoreceptors. At 14 days post injury there were no differences in basal ACh levels. However, injury produced a significant reduction in scopolamine-evoked ACh release. The data suggest that cholinergic neurotransmission remains chronically compromised, and thus may contribute to previously documented post traumatic spatial memory deficits.

Acetylcholine↗