Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. A thiol proteinase from human pituitaries was purified approximately 400 fold and shown to have different chromatographic properties from that of calf brain. Among substrates cleaved were myelin basic protein, histones, beta-lipotropin, neurophysin, and Substance P. 2. The enzyme showed properties associated with a cathepsin-B like enzyme: dependence on -SH groups, pH optimum of 6.5, inhibition by leupeptin and a synthetic analog, Boc-D-Phe-Pro-arginal, and cleavage of dipeptidyl arylamides with basic residues adjacent to or penultimate to the chromatographic grouping. 3. Membranes present in the P2 fraction of rat brain contained three or more enkephalinases when submitted to DEAE-cellulose chromatography. Further purification on an IgG-Sepharose affinity column prepared with antibody to lung angiotensin converting enzyme indicated the presence of dipeptidyl carboxypeptidase(s) with properties distinct from those of ACE. In addition, the DEAE-cellulose fractions contained various aminopeptidase activities when tested with Leu-Gly-Gly, Leu-Nap, and Ala-Ala-Nap as substrates.
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PMID:Peptide processing in the central nervous system. 625 8

The etiology of autism is complex, and in most cases the underlying pathologic mechanisms are unknown. Autism is a hetereogeneous disorder, diagnosed subjectively on the basis of a large number of criteria. Recent research has investigated genetics, in utero insults and brain function as well as neurochemical and immunological factors. On the basis of family and twin studies, there appears to be a genetic basis for a wide "autistic syndrome." About a quarter of cases of autism are associated with genetic disorders such as fragile X syndrome or with infectious diseases such as congenital rubella. Genetic studies have shown an association between autism markers of brain development such as 3 markers of the c-Harvey-ros oncogene and the homeobox gene EN2. In some cases, autism is associated with insults early in gestation, including thalidomide embryopathy. Autism may arise from abnormal central nervous system functioning, since most autistic patients have indications of brain dysfunction, and about half of them have abnormal electroencephalograms. Similarly, the pattern of evoked response potentials and conduction time is altered in autistic children. There is substantial evidence from neuroimaging studies that dysfunctions in the cerebellum and possibly the temporal lobe and association cortex occur in autistic symptoms. Neurochemical studies have investigated the role of serotonin, epinephrine and norepinephrine, since levels of these neurotransmitters are altered in autism, although other hypotheses implicate overactive brain opioid systems and changes in oxytocin neurotransmission. Autoimmunity may also play a role; antibodies against myelin basic protein are often found in children with autism, who also have increased eosinophil and basophil response to IgE-mediated reactions. In summary, the prevailing view is that autism is caused by a pathophysiologic process arising from the interaction of an early environmental insult and a genetic predisposition.
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PMID:Etiology of infantile autism: a review of recent advances in genetic and neurobiological research. 1021 50

A serum-free medium has been devised which permits proliferation of the mouse primitive nervous cell line F7. When cholesterol, eye-derived growth factor and brain extract are added in this medium for 48 h, 80-90% of oligodendrocyte-like cells are generated. These cells have diminished substrate adhesion. They acquire the capacity to synthesize carbonic anhydrase II and myelin basic protein, two specific proteins of oligodendrocytes. These observations suggest that F7 clonal cell line, which has been previously shown to be a neurophysin cell precursor, is also a precursor for oligodendrocytes, and represents a bipotent stem cell line for both neuronal and glial cell lineages.
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PMID:Induction of oligodendrocyte-like properties in a primitive hypothalamic cell line by cholesterol, an eye derived growth factor and brain extract. 1189 26

Six neurohypophysial GCTs and 31 normal neurohypophysis were studied by immunohistochemical techniques. The latter were grouped into A (< 5 yr old), B (30-49 yr), and C (> 70 yr). GCTs were all labeled by PNA, and some showed reactivity for S-100 protein, AAT, AAC, and cathepsin B. In addition, some were oxytocin- and vasopressinpositive. Unlike extracranial GCTs, neuron-specific enolase, myelin basic protein, and vimentin were not detected. Glial fibrillary acidic protein, keratin, and desmin were also not observed. In contrast, a few cells of the normal neurohypophysis showed immunoreactivity for AAT, AAC, cathepsin B, and PNA, similar to the cells of GCT. These cells tended to increase in number with age: group A showed fewer cathepsin B-positive cells than groups B and C (p < 0.001). These results show that neurohypophysial GCTs have some features that differentiate them from extracranial GCTs, for which a Schwann cell origin has been proposed by many authors. It was concluded that neurohypophysial GCT may originate from the cells that showed similar immunoreactivity, the "granular" pituicytes. Our results also support the hypothesis that neurohypophysial GCTs are an age-related metabolic disorder of lysosomes rather than true neoplasms.Endocr Pathol 4:140-145, 1993.
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PMID:Immunohistochemical study of granular cell tumors and granular pituicytes of the neurohypophysis. 3237 Apr 28