Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microtubule-associated protein 2 (MAP-2), a cytoskeletal protein of 280 kilodalton that is highly enriched in dendrites and neuronal perikarya, is subject to both cyclic AMP-, calcium/calmodulin-, and calcium/phospholipid-regulated phosphorylation when incubated with [gamma-32P]ATP in vitro. We have analyzed the different sites in MAP-2 phosphorylated by these three kinases in fresh or boiled cytosol from different regions of the rat brain, in particular the olfactory bulb, where only one form (MAP-2B) is present, and the cerebral cortex, where both forms (MAP-2A and MAP-2B) are equally enriched. Cyclic AMP-dependent protein kinase and calcium/calmodulin-dependent protein kinase II phosphorylated four common phosphorylation sites, as well as a number of distinct sites that were unique to each enzyme. Calcium/phospholipid-dependent protein kinase phosphorylated a minimum of 15 sites, only one of which appeared to be shared with the other protein kinases. Only serine residues were phosphorylated by cyclic AMP-dependent and calcium/phospholipid-dependent protein kinases, while both serine and threonine residues were phosphorylated by calcium/calmodulin-dependent protein kinase II. No differences were observed in the peptide maps of phospho-MAP-2 prepared from different brain regions. These results emphasize the complexity of the phosphorylation systems that may regulate the function of MAP-2 in situ.
J Mol Neurosci 1989
PMID:Multisite phosphorylation of microtubule-associated protein 2 (MAP-2) in rat brain: peptide mapping distinguishes between cyclic AMP-, calcium/calmodulin-, and calcium/phospholipid-regulated phosphorylation mechanisms. 256 75

To investigate patterns of expression of the gene encoding the beta-subunit of S-100 protein during development of the rat brain we have used Northern blotting and in situ hybridization histochemistry. During late prenatal development beta-S-100 mRNA was observed first in the germinal zone lining the 4th ventricle. In the postnatal cerebellum this mRNA accumulated primarily in Bergmann glia and astrocytes of the deep white matter. In the hindbrain, expression of S-100 mRNA increased steadily in specific regions during the first postnatal week while levels remained low in more anterior brain regions. By the end of the second postnatal week, a dense punctate signal was distributed throughout the midbrain and hindbrain. Expression in forebrain, first observed at E18, was confined to cells lining the ventricle until the second postnatal week when accumulation of mRNA was observed in specific regions of the hippocampus, neocortex and olfactory bulb. The adult brain pattern of beta-S-100 mRNA distribution is attained during the third postnatal week. These results demonstrate a caudal-rostral gradient in expression of the beta-S-100 gene during rat brain development, as well as pronounced regional differences which may reflect the differentiation of subpopulations of astrocytes.
Brain Res Mol Brain Res 1989 Dec
PMID:Expression of the gene encoding the beta-subunit of S-100 protein in the developing rat brain analyzed by in situ hybridization. 259 80

The mRNA of rat secretory-vesicle protein chromogranin B is abundant in brain, adrenal medulla, and anterior pituitary. The primary translation product predicted from the cDNA sequence of this 2,337-nucleotide transcript corresponds to a hydrophilic 655-residue protein preceded by a signal peptide. Both termini of the mature 75-kD protein show extensive similarity to other chromogranins; the more variable internal region is characterized by glutamic acid clusters and numerous pairs of basic residues. In rodent brain, mRNA accumulation starts around embryonic days 13-14 and peaks by postnatal day 20. In situ hybridization in brain sections shows that the mRNA is enriched in the hippocampal formation, the endocrine hypothalamus, the olfactory system, and in anatomically distinct structures in the pons-medulla.
J Mol Neurosci 1989
PMID:Nucleotide sequence and cellular distribution of rat chromogranin B (secretogranin I) mRNA in the neuroendocrine system. 264 Dec 78

Kallmann syndrome inherited hypogonadotropic hypogonadism with anosmia, is associated with an X-chromosome deletion at Xp 22.3. In a Kallmann fetus, we have found an absence of luteinizing hormone-releasing hormone (LHRH)-expressing cells in the brain despite dense clusters of LHRH cells and fibers in the nose. LHRH-containing cells and neurites end in a tangle beneath the forebrain, within the dural layers of the meninges, on the dorsal surface of the cribriform plate of the ethmoid bone. Normal fetal brains, matched for age and sex, had LHRH cells and fibers, as expected, in the hypothalamus and preoptic area. Since LHRH-expressing cells recently were discovered to migrate from the olfactory placode into the brain, it appears that the hypogonadotropism of the Kallmann syndrome can be accounted for by a failure of LHRH cells to migrate into the brain.
Brain Res Mol Brain Res 1989 Dec
PMID:Luteinizing hormone-releasing hormone (LHRH)-expressing cells do not migrate normally in an inherited hypogonadal (Kallmann) syndrome. 268 10

We have mapped the distribution of glucocorticoid receptor (GR) mRNA in the male adult rat brain using T7 RNA polymerase transcripts of a 1155 base pair rat GR cDNA clone comprising the coding region for amino acids 140-525. Strong expression of GR mRNA was found in the neurons of the CA1 and CA2 fields of the hippocampus and in the paraventricular and periventricular hypothalamic nuclei. Moderate to strong hybridization was found in the dorsal thalamic nuclei, layers II and VI of the cerebral cortex, the anterior olfactory nucleus and primary olfactory cortex, the hypothalamic mammillary nuclei, the subthalamus, and the granule and mitral cells of the olfactory bulb. Weak to moderate hybridization was found in many other regions of the tel- and diencephalon. Mes- and rhomboencephalic neurons displayed very low levels of GR mRNA relative to the levels observed in the tel- and diencephalon. In the cerebellum, moderate to strong levels of mRNA were detected in the granule and Purkinje cell layers with very low levels elsewhere. Nonneuronal brain elements, such as glial cells, the pia mater, and the choroid plexus, were found to express low to moderate amounts of GR mRNA. These results confirm and extend mapping studies of steroid receptors in the brain using radiolabeled steroids or monoclonal antibodies against rat liver GR and demonstrate that the relative distribution of GR protein in different brain nuclei reflects differences in GR mRNA levels. The rat GR cDNA clone is also shown to provide suitable probes for mapping GR gene expression in the mouse brain.
Mol Endocrinol 1989 Mar
PMID:In situ hybridization mapping of glucocorticoid receptor messenger ribonucleic acid in rat brain. 274 54

Developmental regulation of somatostatin (SRIF) gene expression was studied in five regions of rat brain and in rat stomach. Total RNA was isolated from hypothalamus, cortex, brainstem, cerebellum, and olfactory bulb, as well as stomach at eight stages of development from prenatal day 16 to postnatal day 82. Hybridization of a 32P-labeled rat SRIF cDNA probe to Northern blots of total RNA from the above tissues during development demonstrated a single hybridizing band approximately 670 base pairs in length. When SRIF mRNA levels from each stage of development were quantified and normalized by the amount of poly (A)+ RNA present at that stage of development, a unique pattern of SRIF gene expression was seen in each region. In brainstem and cerebellum, SRIF mRNA levels peaked early in development between prenatal day 21 and postnatal day 8 and then declined until postnatal day 82. Hypothalamus and cortex, on the other hand, showed a progressive increase during development with peak levels occurring between postnatal days 13 and 82. In contrast, stomach and olfactory bulb showed SRIF mRNA levels which were low during early development and which rose late in development (postnatal days 13 to 82). Marked differences in the amount of SRIF mRNA within each region were present as well. These data suggest that there is differential expression of the SRIF gene in different regions of the brain and in the stomach during development. Further study of this phenomenon may provide insight into the in vivo control of SRIF gene expression and the role of SRIF in the developing brain.
Mol Endocrinol 1987 Feb
PMID:Developmental regulation of somatostatin gene expression in the brain is region specific. 290 Oct 33

The effects of single and repeated electroconvulsive shock (ECS) on the binding of [3H]diprenorphine to rat brain membranes was studied. Repeated but not single ECS significantly increased the Bmax of [3H]diprenorphine binding when measured in the absence but not in the presence of NaCl. On a regional basis the effect of ECS was greatest in the olfactory bulb, nucleus accumbens, and striatum. More modest increases were found in the hippocampus, amygdala, septum, hypothalamus, and pyriform cortex. No significant effect was found in the brainstem and frontal cortex. Although the regional rank order of receptor increase does not match the receptor distribution of brain enkephalins, the receptor increase does parallel the regional increases in brain enkephalins following ECS.
Mol Pharmacol 1987 May
PMID:Repeated electroconvulsive shock: effect on sodium dependency and regional distribution of opioid-binding sites. 303 70

A quantitative assessment of the levels of cytochromes P-450 b and P-450 c in the brains and pituitary glands of untreated and beta-naphthoflavone (BNF)-pretreated rats was made with polyclonal antibodies raised against hepatic P-450 b and c and the sensitive fluorometric assay of P-450 catalytic activity, namely, the O-deethylation of ethoxycoumarin (ETC). In the microsomal fraction of brains of untreated rats, the rate of formation of 7-hydroxycoumarin from ETC ranged between 0.1 and 20 pmol/min/mg of microsomal protein, which is approximately 0.01-2% of the level of hepatic microsomes of phenobarbital-induced rats. This brain activity was completely inhibited by anti P-450 b antibodies but was unaffected by anti P-450 c antibodies. As with hepatic P-450 b, metyrapone and chloramphenicol (100 microM) were good inhibitors of catalytic activity, whereas alpha-naphthoflavone (1 microM) was a poor inhibitor. No ETC O-deethylase activity was detectable in microsomes prepared from the pituitary glands of untreated rats. Upon pretreatment of rats with BNF, there was induction of ETC O-deethylase activity in the pituitary gland to a level of 3.3 +/- 1.5 pmol/min/mg of microsomal protein, but there was no significant increase in the level of activity in brain microsomes. Despite this, there was evidence of induction of P-450 c in both the brain and pituitary of BNF-pretreated rats since anti P-450 c antibodies inhibited brain activity by 55% and pituitary activity by 84%. The regional distribution of P-450 b and c in the hypothalamic-preoptic area and olfactory bulbs was examined. The level of ETC O-deethylase activity in the hypothalamic-preoptic area was not different from that in the whole brain, but in the olfactory bulbs activity was higher than that in whole brain, with a range of 0.1-52 pmol/min/mg of microsomal protein. The catalytic activity in the whole brain and in the olfactory bulbs was inhibited by anti P-450b but not by anti P-450c antibodies. Neither estradiol, testosterone, dehydrotestosterone, nor 5 alpha-androstane,3 beta,17 beta-diol (100 microM) competitively inhibited ETC O-deethylase activity, indicating that P-450 b is not responsible for the steroid hydroxylations previously reported in the brain. BNS pretreatment of rats did not cause a consistent increase in ETC O-deethylase upon BNF induction. However, there was an induction of P-450 c in the olfactory bulbs since catalytic activity was inhibited with anti P-450c antibodies.(ABSTRACT TRUNCATED AT 400 WORDS)
Mol Pharmacol 1988 Jan
PMID:Cytochrome P-450 b and c in the rat brain and pituitary gland. 327 64

Aspartate and glutamate are the principal candidates for the excitatory neurotransmitter released by the lateral olfactory tract (LOT) in prepyriform cortex of the rat. Identity of action of the natural transmitter with exogenous glutamate and/or aspartate, however, has not yet been demonstrated. We show that bath-applied 2-amino-4-phosphonobutyric acid, a presumed specific glutamate antagonist, blocks LOT-stimulated prepyriform field potentials and single unit activity but not the single unit response to ionophoretically applied glutamate or aspartate in rat olfactory cortex slices. These results suggest that neither aspartate nor glutamate is the LOT transmitter. Responses to ionophoretically applied N-methyl-DL-aspartate, kainic acid, and DL-homocysteate were clearly decreased by 2-amino-4-phosphonobutyric acid. This suggests that these agents, usually presumed to be aspartate or glutamate agonists, act at different receptors than aspartate and glutamate.
Cell Mol Neurobiol 1981 Mar
PMID:Lateral olfactory tract transmitter: glutamate, aspartate, or neither? 612 64

Mice can recognize the H-2 haplotypes of other mice by scent, and mice show mating preferences for partners of one H-2 type rather than another, usually for partners of an H-2 type different from their own. This olfactory sensing of H-2 odor phenotypes can favor particular H-2 types and promote H-2 diversity, at least under laboratory conditions. This is one reason why we wished to know whether the odor phenotypes of H-2 heterozygotes have distinctive features due to H-2 heterozygosity per se, because such differences could be a further vehicle for reproductive preferences promoting diversity of H-2. A more general reason for interest in the chemosensory individuality of H-2 heterozygotes is that this may shed light on the physical constitution of H-2-related odor phenotypes. The question addressed in this report is whether mice can distinguish the scent of an H-2 heterozygote from the combined scents of the constituent H-2 homozygotes. As in previous studies, the test system employed was the Y maze, in which mice are trained by water deprivation and reward to distinguish the scents of urine samples from alternative panels of donor mice. The critical distinction of the scent of heterozygotes from the combined scents of constituent homozygotes was tested by the transfer-of-training procedure, in which coded urine samples are presented to the trained mice without reward.(ABSTRACT TRUNCATED AT 250 WORDS)
J Mol Cell Immunol 1984
PMID:Chemosensory identity of H-2 heterozygotes. 633 59


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