Insulin receptor substrate (IRS) proteins play a central role in maintaining basic cellular functions such as growth and metabolism. They act as an interface between multiple growth factor receptors possessing tyrosine kinase activity, such as the insulin receptor, and a complex network of intracellular signalling molecules containing Src homology 2 (SH2) domains. Four members (IRS-1, IRS-2, IRS-3, IRS-4) of this family have been identified which differ in their subcellular distribution and interaction with SH2 domain proteins. In addition, differential IRS tissue- and developmental-specific expression patterns may contribute to specificity in their signaling potential.

Adaptor Proteins, Signal Transducing↗

PubMedDate not supplied

Response of insulin receptors to oral glucose in normal subjects.

Insulin binding to circulating monocytes was studied in ten male volunteers before and 1, 2, and 5 hours after the oral intake of 100 g of glucose. Results indicate an increase in the specific cell binding fraction with a change in receptor affinity 5 hours after glucose. Since the same changes appear 3 hours after food intake they are probably not directly induced by insulinemia.

Adult↗

PubMedDate not supplied

B-lipotropin 61-76 and 61-91 fragments act as transglutaminase substrates in vitro.

Both alpha- and beta-endorphin were shown to incorporate radioactive polyamines during incubation in the presence of purified transglutaminase and Ca2+, spermine acting as the best acyl acceptor substrate. The endorphin labelling is dependent on the time of exposure to the enzyme and on the substrate concentration. In the absence of acyl acceptor polyamines, isotopically labelled beta-endorphin gives rise to high molecular weight radioactive polymer(s). Moreover, when different proteins acting as transglutaminase substrates are added, beta-endorphin produces heterologous structures. These data indicate that the glutamine-71 of the beta-lipotropin chain, contained in both alpha- and beta-endorphin, functions as acyl donor substrate for the enzyme and that at least one beta-endorphin lysyl residue can serve as acyl acceptor.

Endorphins↗

PubMedDate not supplied

Transformation of mononuclear phagocytes in vivo and malignant histiocytosis caused by a novel murine spleen focus-forming virus.

The study of retrovirus-induced leukaemias in mice is a powerful tool for the elucidation of the normal regulation of the haematopoietic system. The acute murine spleen focus-forming viruses (SFFV) can be classified according to the haematopoietic lineage on which they exert their effects in the adult mouse. Here we report a new SFFV isolate, the AF-1 virus, with the novel ability to transform cells of the mononuclear phagocyte lineage. The virus was isolated from sarcomas that were induced on passage of a cloned Friend helper virus (F-MuLV, 643/22F) in newborn BALB/c mice. We have cloned the transforming defective subunit of the AF-1 viral complex in NRK cells and isolated several subclones. Analysis of the proviral genome in two non-producer cell clones reveals that AF-1 virus contains Harvey v-ras-specific sequences (Fig. 1). Thus, AF-1 virus is closely related to Harvey murine sarcoma virus (Ha-MSV), and is, at present, the only tool by which permanent cell lines can be obtained from mononuclear phagocytes in the mouse.

Animals↗

PubMedDate not supplied

A new oncogene in human thyroid papillary carcinomas and their lymph-nodal metastases.

Using DNA transfection analysis on NIH 3T3 cells, activated human oncogenes have been isolated from a variety of fresh solid tumours. Thyroid neoplasias show a wide range of lesions varying from slowly progressive well-differentiated tumours to anaplastic highly malignant neoplasms. Therefore they represent an attractive model to investigate the role of oncogene activation in different stages of the neoplastic state. Here we report the detection of transforming activity in DNAs extracted from five thyroid papillary carcinomas and two of their respective lymph-nodal metastases.

Animals↗

PubMedDate not supplied

Stroke in paced patients with sick sinus syndrome: relevance of atrial mechanical function, pacing mode and clinical characteristics.

Patients with sick sinus syndrome have a high prevalence of cerebral ischemia and emboli of the viscera and extremities. The present study was designed to establish the prevalence of stroke in patients with sick sinus syndrome, with specific attention to pacing mode, atrial function (evaluated using Doppler echocardiography) and the clinical condition of the patients. The prospective study analyzed 80 consecutive patients with sick sinus syndrome who received either atrial, dual chamber or ventricular pacemakers. Patients underwent a cranial CT scan at the time of enrollment and again at the end of the study 24 months later. End points of the study were cerebral ischemia or emboli of the viscera or extremities. Clinical and echocardiographic features were assessed at the beginning of the study. A multivariate regression analysis was applied to all variables that had at least a marginal univariate predictive value. Cerebral ischemia occurred in 13 patients and emboli of the viscera or extremities were observed in 2 patients. Univariate predictors for embolism consisted of a prior history of cerebrovascular disease (p < 0.001), low atrial ejection force (p < 0.01) and a dilated left atrium with spontaneous echo contrast (p < 0.05). Independent risk factors for stroke included a history of previous cerebral ischemia, age > 65 years, left atrial echo contrast on an echocardiogram and a depressed atrial ejection force. These findings identified patients at high risk for the development of peripheral embolism among the group of patients paced for sick sinus syndrome.

Adolescent↗

PubMedDate not supplied

Ultrasonography in the evaluation of pleural pathology.

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Humans↗