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At least 127 records · Page 7Linked to original sources
PubMed2003

Ras recruits mitotic exit regulator Lte1 to the bud cortex in budding yeast.

ACdc25 family protein Lte1 (low temperature essential) is essential for mitotic exit at a lowered temperature and has been presumed to be a guanine nucleotide exchange factor (GEF) for a small GTPase Tem1, which is a key regulator of mitotic exit. We found that Lte1 physically associates with Ras2-GTP both in vivo and in vitro and that the Cdc25 homology domain (CHD) of Lte1 is essential for the interaction with Ras2. Furthermore, we found that the proper localization of Lte1 to the bud cortex is dependent on active Ras and that the overexpression of a derivative of Lte1 without the CHD suppresses defects in mitotic exit of a Deltalte1 mutant and a Deltaras1 Deltaras2 mutant. These results suggest that Lte1 is a downstream effector protein of Ras in mitotic exit and that the Ras GEF domain of Lte1 is not essential for mitotic exit but required for its localization.

Cells, Cultured↗
PubMed2006

Exit from mitosis triggers Chs2p transport from the endoplasmic reticulum to mother-daughter neck via the secretory pathway in budding yeast.

Budding yeast chitin synthase 2 (Chs2p), which lays down the primary septum, localizes to the mother-daughter neck in telophase. However, the mechanism underlying the timely neck localization of Chs2p is not known. Recently, it was found that a component of the exocyst complex, Sec3p-green fluorescent protein, arrives at the neck upon mitotic exit. It is not clear whether the neck localization of Chs2p, which is a cargo of the exocyst complex, was similarly regulated by mitotic exit. We report that Chs2p was restrained in the endoplasmic reticulum (ER) during metaphase. Furthermore, mitotic exit was sufficient to cause Chs2p neck localization specifically by triggering the Sec12p-dependent transport of Chs2p out of the ER. Chs2p was "forced" prematurely to the neck by mitotic kinase inactivation at metaphase, with chitin deposition occurring between mother and daughter cells. The dependence of Chs2p exit from the ER followed by its transport to the neck upon mitotic exit ensures that septum formation occurs only after the completion of mitotic events.

Cell Cycle Proteins↗
PubMed2003

The effect of the Varian amorphous silicon electronic portal imaging device on exit skin dose.

Measurements have been made of the increase in exit surface dose resulting from backscattered radiation generated by the Varian amorphous silicon electronic portal imaging device (EPID). An increase of < or = 14% was demonstrated at both 6 MV and 10 MV, in a manner which suggests that backscatter from the EPID acts to re-establish electronic equilibrium at the exit surface, normally absent in the build-down region. The magnitude of this effect was influenced by field size, measurement depth and exit surface to EPID distance. Assuming typical constraints of portal imaging frequency and geometry, the results suggest that EPID generated backscatter is unlikely to alter the frequency or severity of exit skin reactions. However, the results do suggest that a limit on the minimum separation between the EPID and the exit surface should be set, and that similar investigations should be made for other EPID models.

Equipment Failure Analysis↗
PubMed2002

Selective protein exit from yeast endoplasmic reticulum in absence of functional COPII coat component Sec13p.

Sec13p has been thought to be an essential component of the COPII coat, required for exit of proteins from the yeast endoplasmic reticulum (ER). We show herein that normal function of Sec13p was not required for ER exit of the Hsp150 glycoprotein. Hsp150 was secreted to the medium under restrictive conditions in a sec13-1 mutant. The COPII components Sec23p and Sec31p and the GTP/GDP exchange factor Sec12p were required in functional form for secretion of Hsp150. Hsp150 leaves the ER in the absence of retrograde COPI traffic, and the responsible determinant is a peptide repeated 11 times in the middle of the Hsp150 sequence. Herein, we localized the sorting determinant for Sec13p-independent ER exit to the C-terminal domain. Sec13p-dependent invertase left the ER in the absence of normal Sec13p function, when fused to the C-terminal domain of Hsp150, demonstrating that this domain contained an active mediator of Sec13p-independent secretion. Thus, Hsp150 harbors two different signatures that regulate its ER exit. Our data show that transport vesicles lacking functional Sec13p can carry out ER-to-Golgi transport, but select only specific cargo protein(s) for ER exit.

COP-Coated Vesicles↗
PubMed2003

Genetic and biochemical evaluation of the importance of Cdc6 in regulating mitotic exit.

We evaluated the hypothesis that the N-terminal region of the replication control protein Cdc6 acts as an inhibitor of cyclin-dependent kinase (Cdk) activity, promoting mitotic exit. Cdc6 accumulation is restricted to the period from mid-cell cycle until the succeeding G1, due to proteolytic control that requires the Cdc6 N-terminal region. During late mitosis, Cdc6 is present at levels comparable with Sic1 and binds specifically to the mitotic cyclin Clb2. Moderate overexpression of Cdc6 promotes viability of CLB2Deltadb strains, which otherwise arrest at mitotic exit, and rescue is dependent on the N-terminal putative Cdk-inhibitory domain. These observations support the potential for Cdc6 to inhibit Clb2-Cdk, thus promoting mitotic exit. Consistent with this idea, we observed a cytokinesis defect in cdh1Delta sic1Delta cdc6Delta2-49 triple mutants. However, we were able to construct viable strains, in three different backgrounds, containing neither SIC1 nor the Cdc6 Cdk-inhibitory domain, in contradiction to previous work. We conclude, therefore, that although both Cdc6 and Sic1 have the potential to facilitate mitotic exit by inhibiting Clb2-Cdk, mitotic exit nevertheless does not require any identified stoichiometric inhibitor of Cdk activity.

Cell Cycle↗
PubMed2006

The stress-activated mitogen-activated protein kinase signaling cascade promotes exit from mitosis.

In budding yeast, a signaling network known as the mitotic exit network (MEN) triggers exit from mitosis. We find that hypertonic stress allows MEN mutants to exit from mitosis in a manner dependent on the high osmolarity glycerol (HOG) mitogen-activated protein (MAP) kinase cascade. The HOG pathway drives exit from mitosis in MEN mutants by promoting the activation of the MEN effector, the protein phosphatase Cdc14. Activation of Cdc14 depends on the Cdc14 early anaphase release network, a group of proteins that functions in parallel to the MEN to promote Cdc14 function. Notably, exit from mitosis is promoted by the signaling branch defined by the Sho1 osmosensing system, but not by the Sln1 osmosensor of the HOG pathway. Our results suggest that the stress MAP kinase pathway mobilizes programs to promote completion of the cell cycle and entry into G1 under unfavorable conditions.

Cell Cycle↗
PubMed2002

A role for cell polarity proteins in mitotic exit.

The budding yeast mitotic exit network (MEN) is a signal transduction cascade that controls exit from mitosis by facilitating the release of the cell cycle phosphatase Cdc14 from the nucleolus. The G protein Tem1 regulates MEN activity. The Tem1 guanine nucleotide exchange factor (GEF) Lte1 associates with the cortex of the bud and activates the MEN upon the formation of an anaphase spindle. Thus, the cell cortex has an important but ill-defined role in MEN regulation. Here, we describe a network of conserved cortical cell polarity proteins that have key roles in mitotic exit. The Rho-like GTPase Cdc42, its GEF Cdc24 and its effector Cla4 [a member of the p21-activated kinases (PAKs)] control the initial binding and activation of Lte1 to the bud cortex. Moreover, Cdc24, Cdc42 and Ste20, another PAK, probably function parallel to Lte1 in facilitating mitotic exit. Finally, the cell polarity proteins Kel1 and Kel2 are present in complexes with both Lte1 and Tem1, and negatively regulate mitotic exit.

Caenorhabditis elegans Proteins↗
PubMed2002

A defect of Kap104 alleviates the requirement of mitotic exit network gene functions in Saccharomyces cerevisiae.

A subgroup of the karyopherin beta (also called importin beta) protein that includes budding yeast Kap104 and human transportin/karyopherin beta2 is reported to function as a receptor for the transport of mRNA-binding proteins into the nucleus. We identified KAP104 as a responsible gene for a suppressor mutation of cdc15-2. We found that the kap104-E604K mutation suppressed the temperature-sensitive growth of cdc15-2 cells by promoting the exit from mitosis and suppressed the temperature sensitivity of various mitotic-exit mutations. The cytokinesis defect of these mitotic-exit mutants was not suppressed by kap104-E604K. Furthermore, the kap104-E604K mutation delays entry into DNA synthesis even at a permissive temperature. In cdc15-2 kap104-E604K cells, SWI5 and SIC1, but not CDH1, became essential at a high temperature, suggesting that the kap104-E604K mutation promotes mitotic exit via the Swi5-Sic1 pathway. Interestingly, SPO12, which is involved in the release of Cdc14 from the nucleolus during early anaphase, also became essential in cdc15-2 kap104-E604K cells at a high temperature. The kap104-E604K mutation caused a partial delocalization of Cdc14 from the nucleolus during interphase. This delocalization of Cdc14 was suppressed by the deletion of SPO12. These results suggest that a mutation in Kap104 stimulates exit from mitosis through the activation of Cdc14 and implies a novel role for Kap104 in cell-cycle progression in budding yeast.

Base Sequence↗
PubMed1995

The effects of visual barriers on exiting behavior in a dementia care unit.

Exiting due to wandering was a problem for caregivers in this dementia care unit. Previous attempts to control exiting by wanderers proved ineffective. We manipulated the view and light through a window using visual barriers: window blind, cloth barrier, and a combination of the two. The closed blind reduced exiting by 44%. The cloth barrier was the most effective solution, reducing exiting by 96%. The combination of the blind and cloth barrier reduced exiting 88%. These findings support those of Namazi, Rosner, and Calkins (1989).

Aged↗
PubMed1995

Cuff-shaving procedure. A rescue treatment for exit-site infection unresponsive to medical therapy.

We performed 41 cuff-shaving procedures in 38 patients on continuous ambulatory peritoneal dialysis (CAPD) with exit-site infection unresponsive to medical treatment. Cuff shaving was performed on three patients with two catheters each. This procedure was effective in eliminating 50% of S. aureus exit-site infection and all S. epidermidis exit-site infection, but was ineffective in Gram-negative exit-site infection. After cuff-shaving procedure, 20 catheters (49%) were removed; 11 for persistent tunnel infection and nine because of development of secondary peritonitis. The probability of catheter survival at 1 year was 50% and remained stable thereafter. Cuff-shaving procedure may be a valuable mode of therapy for treating patients with S. aureus and/or S. epidermidis exit-site infection unresponsive to medical treatment.

Anti-Bacterial Agents↗
PubMed2000

Incomplete shored exit wounds: a report of three cases.

Typical and atypical exit wounds are well described in the forensic literature. Included in the descriptions of atypical exit wounds are perforating, "shored" exit wounds, in which the perforation of the skin is associated with an abrasion, whether or not the bullet fully exits the body. The authors describe an atypical, incomplete, shored exit wound in which the skin was abraded by supporting material at the site the bullet was recovered, but there was no associated perforation of the skin. Recognition of this injury pattern can be important in reconstruction of the crime scene in relation to the victim at the time of the shooting.

Adult↗
PubMedDate not supplied

Progress in the moral reasoning of baccalaureate nursing students between program entry and exit.

Changes in moral reasoning between entry into and exit from a baccalaureate nursing program and the relationship between student characteristics and moral reasoning at entry and exit were explored in this descriptive study. The moral reasoning of four cohorts of students was measured using the Defining Issues Test (DIT). Admission grade point average, prior college credits, and gender accounted for 10% of the variance in DIT P% scores at entry and 14% of the variance at exit from the program. Female students had significantly higher moral reasoning scores than men. Age did not contribute significantly to explaining DIT score variance. DIT P% scores at entry for all four cohorts were within the range of reported norms for college students. Exit scores for all four cohorts were between the normative means for undergraduate students and graduate students. DIT P% score gains between entry and exit were significant for all four cohorts. Students whose entry scores were in the lowest categories had the greatest mean gains.

Adult↗
PubMed1979

Studies on amino acid inhibition of monosaccharide exit from anuran small intestinal epithelium.

1. The effect of the addition of amino acids to the intestinal lumen upon the movement of the monosaccharide alpha-methyl-D-glucopyranoside (alpha MG) from the preloaded epithelium into the blood and into the lumen of the vascularly perfused frog small intestine has been studied. 2. The neutral hydrophobic amino acids tryptophan, leucine, phenylalanine, tyrosine, isoleucine, valine, norleucine and cycloleucine all rapidly inhibit the exit of alpha MG out of the epithelium into the vascular bed. They stimulate backflux of the sugar from the epithelium into the lumen to a very much smaller extent. 3. L-Leucine is a more effective inhibitor of alpha MG exit into the blood than is D-leucine. Near-maximal inhibition of alpha MG exit is seen with 10 mM-L-leucine in the intestinal lumen. 4. The addition of leucine (10 mM) to the lumen of the intestine preloaded with alpha MG approximately halves the rate constant for alpha MG washout into the blood from 12.6 +/- 1.7 (4) x 10(-3) to 5.5 +/- 1.4 (4) x 10(-3) min-1, without appreciably altering the pool of monosaccharide in the tissue. The inhibitory effect of L-leucine upon alpha MG exit into the blood is not abolished by the presence of phlorizin (5 x 10(-5) M) in the intestinal lumen. 5. The complex pattern of inhibition of alpha MG transfer from the lumen to the blood observed upon the addition of L-leucine to the lumen is consistent with the finding that the amino acid inhibits the exit of the monosaccharide out of the epithelium into the blood in addition to any inhibitory effect upon sugar entry across the brush border. 6. It is suggested that alpha MG may be a substrate for a proposed transport system for neutral hydrophobic amino acids which, it is suggested, is present in the basolateral membrane of the epithelial cell.

Amino Acids↗
PubMed1982

Amino acid inhibition and stimulation of 2-aminoisobutyric acid exit from anuran small intestine.

1. Using the vascularly perfused frog small intestine, the exit of the non-metabolized amino acid 2-aminoisobutyric acid (AIB) from the pre-loaded epithelium into the blood has been studied in winter animals.2. Marked inhibition of the instantaneous rate constant for AIB exit into the vascular bed is observed when L-leucine, but not D-leucine, is added either to the intestinal lumen or to the vascular bed. The extent of the inhibition is related to the leucine concentration in an alinear fashion. The concentration of luminal L-leucine giving half maximal inhibition is 2.5 mM.3. The instantaneous rate constant for AIB exit is similarly decreased by 10 mM-L-tryptophan and by L-phenylalanine added to the intestinal lumen and to a lesser extent by L-asparagine, L-valine, L-glutamine, L-isoleucine, and L-norleucine.4. 10 mM-L-proline added to the lumen stimulates AIB exit from the pre-loaded epithelium into the blood. This stimulation is due to an increased rate constant for movement of AIB across the basolateral membrane.5. No inhibition is found when the dipeptide L-leucyl-L-leucine (10 mM) is added to the intestinal lumen in the presence of 10 mM-L-leucine. When added to the vascular compartment this dipeptide has no effect upon AIB exit from the epithelium.6. Possible mechanisms by which amino acids and peptides may influence AIB movement out of the epithelium into the blood are discussed and conclusions are drawn concerning AIB transport across the intestinal basolateral membrane of the intact epithelium.

Amino Acids↗
PubMed1997

A convolution model to convert transmission dose images to exit dose distributions.

The aim of this study is to develop a model which computes exit dose values from transmission dose data obtained during patient treatment with an electronic portal imaging device (EPID). The proposed model convolves the primary dose distribution, derived from transmission dose distributions at large air gaps, with a scatter kernel to obtain the exit dose. The influence of inhomogeneities on the scatter contribution is taken into account by using a radiological path length model. To determine the parameters of the model, an extensive set of transmission dose measurements was performed behind various phantoms in an 8 MV beam using a liquid-filled EPID. The influence on the transmission dose of field size, phantom thickness, air gap between phantom and detector, and source-phantom distance was investigated. At air gaps larger than 50 cm the distribution of scattered dose is almost flat and its contribution to the total dose is relatively small, thus allowing an accurate separation of the primary and scattered dose by subtraction. Scattered dose distributions for air gaps smaller than 50 cm were obtained by subtracting the primary dose (corrected for divergence) from the measured total transmission dose. The resulting scattered dose distribution behind homogeneous phantoms has a Gaussian shaped profile, which becomes wider with increasing air gap. The relative contribution of scattered dose depends on the phantom thickness and is maximal for a thickness of about 10 cm. Using these results, the parameters of the convolution model (i.e., the shape of the scatter kernel) were determined. With the model the absolute exit dose is predicted with an accuracy of about 2% (1 s.d.) within the entire radiation field for homogeneous phantoms. Inhomogeneities are taken into account by calculating the radiological path length from the measured primary dose, i.e., without using CT data. By using the measured radiological path length the exit dose can be determined for inhomogeneous phantoms with an accuracy of 2.5%. It is concluded that, using our convolution model, EPID measurements at large air gaps can be used to estimate absolute exit doses in an 8 MV beam with an accuracy of 2.5%.

Algorithms↗
PubMed1984

Mechanism of bicarbonate exit across basolateral membrane of the rabbit proximal convoluted tubule.

To clarify the mechanism(s) of HCO-3 movement across the basolateral membrane, rabbit proximal convoluted tubules were perfused in vitro. Two possible mechanisms were examined: neutral HCO-3 exit coupled to chloride and rheogenic HCO-3 exit. A complete C1- substitution with isethionate in the lumen and bath did not affect HCO-3 reabsorption, suggesting that HCO-3 exit is not coupled to chloride. Addition of 2 mM Ba2+ to the bath, which has been shown to depolarize the basolateral membrane potential difference, caused a 42% inhibition of HCO-3 reabsorption and a 32% inhibition of volume flux, suggesting that HCO-3 exit is rheogenic. Ba2+ did not affect the volume flux when HCO-3 reabsorption was inhibited by acetazolamide, suggesting that the Ba2+ effect is not due to a general inhibition of cell metabolism. From these data we propose that HCO-3 exits the basolateral membrane by a rheogenic, chloride-independent mechanism.

Animals↗
PubMed2006

Exit interview-consultation for research validation and dissemination.

Dissemination of research findings to practice and maintenance of rigor and validity in qualitative research are continuing challenges for nurse researchers. Using three nursing home case studies as examples, this article describes how exit interview-consultation was used as (a) a validation strategy and (b) a rapid research dissemination tool that is particularly useful for nursing systems research. Through an exit interview-consultation method, researchers validated inferences made from qualitative and quantitative data collected in three comprehensive nursing home case studies that examined nursing management practices. This exit interview-consultation strategy extends the traditional member-check approach by providing confirmation at the individual and organizational level. The study examined how using the exit interview-consultation strategy can potentially assist nursing home organizations to increase their capacity for improving operations. Benefits from research participation are often indirect; this study's results suggest that exit interview-consultation can provide direct and immediate benefits to organizations and individuals.

Consultants↗
PubMed2005

The hedgehog-PKA pathway regulates two distinct steps of the differentiation of retinal ganglion cells: the cell-cycle exit of retinoblasts and their neuronal maturation.

In the developing zebrafish retina, neurogenesis is initiated in cells adjacent to the optic stalk and progresses to the entire neural retina. It has been reported that hedgehog (Hh) signalling mediates the progression of the differentiation of retinal ganglion cells (RGCs) in zebrafish. However, the progression of neurogenesis seems to be only mildly delayed by genetic or chemical blockade of the Hh signalling pathway. Here, we show that cAMP-dependent protein kinase (PKA) effectively inhibits the progression of retinal neurogenesis in zebrafish. Almost all retinal cells continue to proliferate when PKA is activated, suggesting that PKA inhibits the cell-cycle exit of retinoblasts. A cyclin-dependent kinase (cdk) inhibitor p27 inhibits the PKA-induced proliferation, suggesting that PKA functions upstream of cyclins and cdk inhibitors. Activation of the Wnt signalling pathway induces the hyperproliferation of retinal cells in zebrafish. The blockade of Wnt signalling inhibits the PKA-induced proliferation, but the activation of Wnt signalling promotes proliferation even in the absence of PKA activity. These observations suggest that PKA inhibits exit from the Wnt-mediated cell cycle rather than stimulates Wnt-mediated cell-cycle progression. PKA is an inhibitor of Hh signalling, and Hh signalling molecule morphants show severe defects in cell-cycle exit of retinoblasts. Together, these data suggest that Hh acts as a short-range signal to induce the cell-cycle exit of retinoblasts. The pulse inhibition of Hh signalling revealed that Hh signalling regulates at least two distinct steps of RGC differentiation: the cell-cycle exit of retinoblasts and RGC maturation. This dual requirement of Hh signalling in RGC differentiation implies that the regulation of a neurogenic wave is more complex in the zebrafish retina than in the Drosophila eye.

Animals↗