Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:O76050 (neu)
 3,969 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Trk immunoreactivity is expressed by a discrete population of cortical neurons, primarily those with cell bodies in layer Vb and dendrites in supragranular cortex. We tested the hypothesis that neurons co-express multiple isoforms of trk receptors. The distribution of neurons expressing specific high affinity neurotrophin receptors was determined immunohistochemically. Multiple antibodies directed against each trk isoform and an antibody directed against an epitope shared by all three trk isoforms were used. The distribution of neurons expressing each of the three receptors was virtually identical. Each anti-trk antibody primarily labeled neurons with cell bodies in layer V. More than one-third of layer V neurons was positive for a high affinity trk receptor. Few immunoreactive somata (1%-5%) were in the other layers. In addition, the neuropil in the supragranular laminae was immunopositive for each trk isoform. Recent data show that layer V neurons in the mature somatosensory cortex express the tyrosine kinase receptor c-erbB2, also known as c-neu. Immunofluorescence double labeling shows that approximately 80% of the c-neu-immunolabeled neurons in layer V co-expressed pan-trk immunoreactivity and two-thirds of all c-neu-positive neurons expressed a specific trk isoform. We concluded from these data that there is significant co-expression of trk isoforms in layer V neurons. In summary, trkA, trkB, trkC, and c-neu were primarily expressed by cortical projection neurons in layer V and co-expression among these receptors was common. This implies that cortical growth factor systems are redundant and that cortical neurons are responsive to more than one growth factor.
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PMID:Neurotrophin receptors in the somatosensory cortex of the mature rat: co-localization of p75, trk, isoforms and c-neu. 1067 63

Breast cancer is the most common cancer in Western women and while its precise etiology is unknown, environmental factors are thought to play a role. The organochlorine pesticide dieldrin is a persistent environmental toxicant thought to increase the risk of breast cancer and reduce survival in the human population. The objective of this study was to define the effect of developmental exposure to environmentally relevant concentrations of dieldrin, on mammary tumor development in the offspring. Sexually mature FVB-MMTV/neu female mice were treated with vehicle (corn oil), or dieldrin (0.45, 2.25, and 4.5 microg/g body weight) daily by gavage for 5 days prior to mating and then once weekly throughout gestation and lactation until weaning. Dieldrin concentrations were selected to produce serum levels representative of human background body burdens, occupational exposure, and overt toxicity. Treatment had no effect on litter size, birth weight or the number of pups surviving to weaning. The highest dose of dieldrin significantly increased the total tumor burden and the volume and number of tumors found in the thoracic mammary glands. Increased mRNA and protein expression of the neurotrophin BDNF and its receptor TrkB was increased in tumors from the offspring of dieldrin treated dams. This study indicates that developmental exposure to the environmental contaminant dieldrin causes increased tumor burden in genetically predisposed mice. Dieldrin exposure also altered the expression of BNDF and TrkB, novel modulators of cancer pathogenesis.
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PMID:Developmental and lactational exposure to dieldrin alters mammary tumorigenesis in Her2/neu transgenic mice. 1917 4