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J E McConnell

Publications and source records attributed to J E McConnell.

7 recordsLinked to original sources
PubMed1995

An astrocytic binding site for neuronal Thy-1 and its effect on neurite outgrowth.

Thy-1, a member of the immunoglobulin superfamily, is one of the most abundant glycoproteins on mammalian neurons. Nevertheless, its role in the peripheral or central nervous system is poorly understood. Certain monoclonal antibodies to Thy-1 promote neurite outgrowth by rodent central nervous system neurons in vitro, suggesting that Thy-1 functions, in part, by modulating neurite outgrowth. We describe a binding site for Thy-1 on astrocytes. This Thy-1-binding protein has been characterized by immunofluroesence with specific anti-idiotype monoclonal antibodies and by three competitive binding assays using (i) anti-idiotype antibodies, (ii) purified Thy-1, and (iii) Thy-1-transfected cells. The Thy-1-binding protein may participate in axonal or dendritic development in the nervous system.

Animals↗
PubMed1995

The mouse 14-3-3 epsilon isoform, a kinase regulator whose expression pattern is modulated in mesenchyme and neuronal differentiation.

Kidney development is a complex, little understood process based on inductive interactions and intricate epithelial and mesenchymal morphogenesis. Here, we report the use of subtractive hybridization to clone cDNAs expressed in early nephrogenesis. cDNA made from E14.5 mouse kidney was hybridized with adult mouse liver mRNA employing a technique based on labeling the driver mRNA with photoactivatable biotin and using streptavidin to remove RNA:cDNA complexes. An aliquot of the unhybridized cDNA identified several clones including three isolates that proved to be the epsilon isoform of the 14-3-3 gene family that is, among other functions, implicated in protein kinase C regulation. Northern blot analysis showed a 2.0-kb transcript widely present in mouse embryos from E7.5 onward, but, as expected from the subtractive strategy, absent in adult liver. In situ hybridization was carried out on mouse embryos aged E8.5 to E15.5. These showed that, in the E8.5 embryo, the 14-3-3 epsilon gene was expressed throughout the embryo, but that, within a day, expression was more marked in mesenchyme than elsewhere (e.g., epithelial tissue, where it was generally low), although levels in neural tissue rose again by about E12.5. This difference was maintained until E15.5 when expression levels started to drop in most tissues, with those of the nervous system, tooth, and kidney being exceptions. Perhaps the most intriguing feature of the expression pattern, however, was that, while the gene was strongly expressed in early mesenchyme, the level of expression decreased as the mesenchyme differentiated. This change was particularly noted in mesenchymal condensations that would become cartilage, bone, and myotome-derived muscle, in the presumptive muscle layer of the gut, and in the kidney. In this last case, the gene was strongly expressed in stem cells and mesenchyme, but expression levels dropped markedly as early nephrogenic condensates epithelialized. The results as a whole thus argue for the 14-3-3 epsilon isoform playing roles in neural development and in early mesenchyme, with this latter function being lost or replaced as the tissue differentiates.

14-3-3 Proteins↗
PubMed1994

Towards a genetic basis for kidney development.

Although it is not easy to investigate the regulatory basis of developmental processes in most mammalian tissues, the mouse kidney has several distinct advantages as a model system. Its development involves a wide variety of developmental processes that include induction, stem-cell regulation, a mesenchyme-to-epithelium transition, epithelial morphogenesis and pattern formation. Further, there are several genetic disorders associated with its development, much of nephrogenesis will take place in vitro and a significant start has been made in elucidating the regulatory molecules involved in its ontogeny. Here, we summarise current knowledge on how the various aspects of kidney development are controlled at the genetic level. For this, we have compiled a table showing when and where the more than forty regulatory genes thus far identified are expressed during nephrogenesis (this table being a subset of a database also containing information on structural and functional proteins expressed during nephrogenesis). The data on the regulatory genes demonstrate, in particular, the importance of the Wilms' tumour gene, WT1, in nephrogenesis, the growth-stimulating interaction between the hepatocyte growth factor and its receptor, c-met, and the differences between uninduced and induced metanephric mesenchyme. In an attempt to highlight those stable developmental pathways which underpin the formation of the kidney and to facilitate future work, we have identified possible checkpoints occurring during nephrogenesis (stages at which a positive signal is needed for development to continue). The data to hand suggest that such checkpoints occur when metanephric mesenchyme is established in the intermediate mesoderm, when induction takes place, when stem cells are activated and before mesenchyme aggregates to form nephrogenic condensations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

The alternative 5'-end of the Drosophila melanogaster epidermal growth factor receptor cDNA (DER) is part of the D14-3-3 cDNA.

A portion of the cDNA reported as a novel cDNA encoding the Drosophila melanogaster homolog of the bovine 14-3-3 protein by Swanson and Ganguly [Gene 113 (1992) 183-190] already exists in the database. It was originally reported as an alternative 5' end of the D. melanogaster homolog of the epidermal growth factor receptor (DER). Schejter and Shilo [Cell 56 (1989) 1093-1164] later reported that this finding was due to a cloning artifact that joined the 14-3-3 cDNA onto the DER cDNA.

14-3-3 Proteins↗
PubMed1972

Issues in health.

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Delivery of Health Care↗
PubMedDate not supplied

Results of diagnostic investigations and long-term outcome of 33 dogs with brain infarction (2000-2004).

Medical records of 33 dogs presented for acute onset, nonprogressive, intracranial dysfunction that had a magnetic resonance imaging diagnosis of brain infarction were reviewed. Postmortem confirmation of brain infarction was available in 10 dogs. All dogs were evaluated by CBC, serum biochemistry, thyroid and adrenal testing, urinalysis, thoracic and abdominal imaging, and cerebrospinal fluid analysis. Results of coagulation profile and arterial blood pressure were available in 32/33 and 28/33 dogs, respectively. On the basis of the imaging findings, infarcts were classified depending on their type (territorial or lacunar) and location within the brain (telencephalic, 10/33; thalamic/midbrain, 8/33; cerebellar, 15/33). No marked associations among location or type of infarct and patient age and sex, occurrence of systemic hypertension, and the presence or absence of a concurrent medical condition were identified. Small breed dogs (< or =15 kg) were significantly more likely to have territorial cerebellar infarcts, whereas large breed dogs (>15 kg) were significantly more likely to have lacunar thalamic or midbrain infarcts. A concurrent medical condition was detected in 18/33 dogs with brain infarcts, with chronic kidney disease (8/33) and hyperadrenocorticism (6/ 33) being most commonly encountered. Of 33 dogs, 10 were euthanized because of the severity and lack of improvement of their neurologic status or the severity of their concurrent medical condition. No association was identified between type or location of infarct and patient outcome. Dogs with concurrent medical conditions had significantly shorter survival times than those with no identifiable medical condition and were significantly more likely to suffer from recurrent neurologic signs because of subsequent infarcts.

Animals↗