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Results for “Functional potential”

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At least 145 records · Page 8Linked to original sources

PubMed1998

Impairment of survival factor function potentiates chemotherapy-induced apoptosis in tumor cells.

The balance between tumor cell proliferation and apoptosis is a critical determinant of malignant tumor outgrowth. In a transgenic mouse model of beta cell tumorigenesis (Rip1Tag2), insulin-like growth factor II (IGF-II) is up-regulated during the onset of tumor cell proliferation. Disruption of IGF-II expression in these transgenic mice causes a dramatic increase of beta tumor cell (betaTC) apoptosis, indicating that IGF-II acts as a survival factor. Here we report that beta tumor cell lines derived from IGF-II-deficient Rip1Tag2 mice show a higher incidence of apoptosis than their wild-type counterparts. In particular, IGF-II-deficient betaTCs are more sensitive to apoptotic stimuli, such as serum deprivation and staurosporine, and to chemotherapeutic agents, such as daunomycin, etoposide, or vincristine. Thus, the lack of the survival factor IGF-II potentiates chemotherapeutic treatment of betaTCs. Furthermore, normal betaTCs can be sensitized to chemotherapy when transfected with a dominant-negative mutant of the IGF-I receptor. These results demonstrate a pivotal role for IGF-mediated signaling in the survival of tumor cells and, thus, raise the possibility of novel approaches toward cancer therapy by interfering with survival factor function.

Animals↗

PubMedDate not supplied

Expression and potential function of Rho family small G proteins in cells of the mammalian seminiferous epithelium.

Dynamic cellular rearrangements involving the actin cytoskeleton are required of both Sertoli and germ cells during spermatogenesis. Rho family small G proteins have been implicated in the control of the actin cytoskeleton in numerous cell types. Therefore, RhoA and Rac1 were investigated in Sertoli and germ cells. RhoA and Rac1 have been detected at both the mRNA and protein levels in these cells. In addition, Sertoli cell L-selectin is shown to interact with actin binding proteins, potentially providing a link between L-selectin and Rac1 signaling. Finally, inactivation of Sertoli cell Rho family proteins yields disruption of the actin cytoskeleton.

Animals↗

PubMed2005

Potential functional neural repair with grafted neural stem cells of early embryonic neuroepithelial origin.

The fate of grafted neuroepithelial stem cells in the normal mature brain environment was assessed both morphologically and electrophysiologically to confirm their feasibility in the functional repair of damaged neural circuitry. The neuroepithelial stem cells were harvested from the mesencephalic neural plate of transgenic green fluorescence protein-carrying rat embryos, and implanted into the normal adult rat striatum. The short- and long-term differentiation pattern of donor-derived cells was precisely monitored immunohistochemically. The functional abilities of the donor-derived cells and communication between them and the host were investigated using host-rat brain slices incorporating the graft with whole-cell patch-clamp recording. Vigorous differentiation of the neuroepithelial stem cells into mostly neurons was noted in the short-term with positive staining for tyrosine hydroxylase, suggesting that the donor-derived cells were exclusively following their genetically programmed fate, together with gamma-aminobutyric acid (GABA) and glutamate expression. In the long-term, the large number of donor-derived neurons was sustained, but the staining pattern showed expression of dopamine- and adenosine 3':5'-monophosphate-regulated phosphoprotein 32, suggesting that some neurons were following environmental cues, together with the appearance of some cholinergic neurons. Some donor-derived astrocytes were also seen in the graft. Many action potentials indicating the presence of both dopaminergic and non-dopaminergic patterns could be elicited and recorded in the donor-derived neurons in addition to spontaneous glutamatergic and GABAergic post-synaptic currents which were strongly shown to be of host origin. Neuroepithelial stem cells are therefore an attractive candidate as a source of donor material for intracerebral grafting in functional repair.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2005

Dietary fats, teas, dairy, and nuts: potential functional foods for weight control?

Functional foods are similar to conventional foods in appearance, but they have benefits that extend beyond their basic nutritional properties. For example, functional foods have been studied for the prevention of osteoporosis, cancer, and cardiovascular disease. They have yet to be related to the prevention of obesity, although obesity is one of the major health problems today. The inclusion of foods or the replacement of habitual foods with others that may enhance energy expenditure (EE) or improve satiety may be a practical way to maintain a stable body weight or assist in achieving weight loss; such foods may act as functional foods in body weight control. Some foods that might be classified as functional foods for weight control because of their effects on EE and appetite-including medium-chain triacylglycerols, diacylglycerols, tea, milk, and nuts-are reviewed here. Only human studies reporting EE, appetite, or body weight are discussed. When studies of whole food items are unavailable, studies of nutraceuticals, the capsular equivalents of functional foods, are reviewed. To date, dietary fats seem to be most promising and have been the most extensively studied for their effects on body weight control. However, the weight loss observed is small and should be considered mostly as a measure to prevent weight gain. Carefully conducted clinical studies are needed to firmly ascertain the effect of tea, milk, and nuts on body weight maintenance, to assess their potential to assist in weight-loss efforts, and to ascertain dose-response relations and mechanisms of action for the 4 food types examined.

Animals↗

PubMed2004

The mechanism of biogenesis and potential function of the two alternatively spliced mRNAs encoded by the murine Msx3 gene.

The homeodomain-containing Msx3 gene, the newest member of the Msx family, encodes two mRNAs, with an unknown relationship to each other. To elucidate how Msx3 gene generates the two transcripts, we cloned their corresponding cDNAs from an E10.5 mouse embryo cDNA library. The alignment of sequences of the two Msx3-specific cDNAs with the corresponding regions of the genomic DNA revealed that read-through of the sequences preceding a cryptic splice donor site in the first intron of Max3 gene generated the longer transcript. The longer Msx3 mRNA (Msx3-l) contains 66 nucleotides spliced in frame that would encode a protein with 22 additional amino acids. These extra 22 amino acids are inserted between the residues 72 and 73, exactly 14 amino acids upstream of the homeodomain of the smaller Msx3 protein. In situ hybridization and competitive RT-PCR experiments revealed that both Msx3-s and Msx3-l mRNAs elicited similar spatio-temporal patterns of expression in the developing embryo, with maximal expression of both mRNAs occurring in the embryos between 8.5 and 12.5 days post-coitus. We found that while Msx3-s down-regulated Msx1 promoter in transfected C2C12 cells, co-expression of Msx3-l alone did not affect the activity of the Msx1 promoter. In contrast, a concomitant expression of Msx3-s and Msx3-l in the transfected C2C12 cells neutralized the repressive effect of Msx3-s on the Msx1 promoter. In transient expression assays, the repressive action of Msx3-s on Msx1 promoter could also be reversed by co-expression of exogenous Sp1. Our data indicate that the potential interactions among the protein products encoded by the alternately spliced Msx3 mRNAs and the putative constituents of transcriptional co-activators and co-repressors may have functional consequences in vivo.

Alternative Splicing↗

PubMed2004

Effects of human immunodeficiency virus type 1 on astrocyte gene expression and function: potential role in neuropathogenesis.

Neurodegeneration and dementia caused by human immunodeficiency virus type 1 (HIV-1) infection of the brain are common complications of acquired immunodeficiency syndrome (AIDS). Introduction of highly active antiretroviral therapy (HAART) reduced the incidence of HIV-1-associated dementia, but so far had no effect on the high frequency of milder neurological disorders caused by HIV-1. This indicates that some neuropathogenic processes persist during limited HIV-1 replication in the central nervous system (CNS). The authors are evaluating the hypothesis that interaction of HIV-1 with astrocytes, which bind HIV-1 but support limited productive HIV-1 infection, may contribute to these processes by disrupting astrocyte functions that are important for neuronal activity or survival. Using laser-capture microdissection on brain tissue samples from HIV-1-infected individuals, we found that HIV-1 DNA can be detected in up to 1% of cortical and basal ganglia astrocytes, thus confirming HIV-1 infection in astrocytes from symptomatic patients. Using rapid subtraction hybridization, the authors cloned and identified 25 messenger RNAs in primary human fetal astrocytes either up-regulated or down-regulated by native HIV-1 infection or exposure to gp120 in vitro. Extending this approach to gene microarray analysis using Affymetrix U133A/B gene chips, the authors determined that HIV-1 alters globally and significantly the overall program of gene expression in astrocytes, including changes in transcripts coding for cytokines, G-coupled protein receptors, transcription factors, and others. Focusing on a specific astrocyte function relevant to neuropathogenesis, the authors showed that exposure of astrocytes to HIV-1 or gp120 in vitro impairs the ability of the cells to transport L-glutamate and the authors related this defect to transcriptional inhibition of the EAAT2 glutamate transporter gene. These findings define new pathways through which HIV-1 may contribute to neuropathogenesis under conditions of limited virus replication in the brain.

AIDS Dementia Complex↗

PubMed1998

The effect of chloride concentration on human neutrophil functions: potential relevance to cystic fibrosis.

Recently, some investigators have observed elevated concentrations of chloride in the airway surface fluid (ASF) overlying respiratory epithelia from cystic fibrosis (CF) patients compared with ASF overlying non-CF epithelia. Others have shown that this elevated ASF salt concentration can inactivate human beta-defensin-1, an antimicrobial peptide secreted by respiratory epithelia. This could impair the primary epithelial defense against bacteria in the CF airway, thereby forcing a greater reliance on polymorphonuclear leukocyte (PMN)-mediated defenses. Pseudomonas aeruginosa (Psa) flourishes in the CF airway despite the presence of abundant PMN. We therefore investigated whether elevated ASF chloride concentration in CF might also compromise PMN function. We employed a cell-culture model in which halide concentrations and osmolarity were varied independently. We examined the effects of chloride concentration on three aspects of PMN function: recruitment of PMN to the airway (production of interleukin-8 [IL-8]), PMN antimicrobial activity (killing of Psa), and PMN clearance from the airways (apoptosis and lysis). We found that exposure to elevated chloride concentration increased PMN synthesis of IL-8, decreased PMN killing of Psa, and accelerated PMN apoptosis and lysis. In CF airways, elevated chloride therefore could contribute to the increased number of PMN recruited into the airways, the increased survival of Psa, and the increased quantity of toxic mediators released by PMN into the airways. These effects of elevated chloride on PMN function may provide another causal link between loss of cystic fibrosis transmembrane conductance regulator function and CF lung disease.

Adult↗

PubMed1995

[The effect of earlier acute diseases on body functional potentials and work capacity].

The study revealed lower Vital Lung Capacity, reduced efficiency of breathing and circulation, aerobic resources and performance in young workers engaged into nonwoven materials production, who had acute respiratory infections and tonsillitis. For better health of the workers prophylaxis of the most prevalent respiratory infections is essential.

Acute Disease↗

PubMed1999

The insulin-like growth factors (IGF) and IGF type I receptor during postnatal growth of the murine mammary gland: sites of messenger ribonucleic acid expression and potential functions.

The goals of this study were to determine the cellular sites of insulin-like growth factor (IGF) and IGF type-I receptor (IGF-IR) expression and to begin to elucidate functional roles for the IGFs during postnatal development of the murine mammary gland. Using in situ hybridization analyses, we determined that IGF-I, IGF-II, and IGF-IR messenger RNAs were expressed in the highly proliferative terminal end buds during pubertal ductal growth. Consistent with these data, IGF-I (in combination with mammogenic hormones) promoted ductal growth in pubertal stage mammary glands cultured in vitro. During postpubertal and pregnancy stages, IGF-II and IGF-IR continued to be expressed in ductal epithelium. Expression of IGF-II in ductal and alveolar epithelium correlated with the pattern of rapidly proliferating cells, as determined by incorporation of 5-Bromo-2'-deoxyuridine, suggesting a potential autocrine or paracrine role for IGF-II as a mitogen for ductal epithelial cells. IGF-I expression was reinitiated in mammary epithelium in the differentiated alveoli at the end of pregnancy, suggesting an additional role for this factor in maintenance of the alveoli during lactation. Taken together, these data support an in vivo role for locally-produced IGFs in promoting ductal growth during puberty and suggest that IGF-I and IGF-II may have distinct functions during pregnancy-induced alveolar development.

Animals↗

PubMed1996

Positive selection moments identify potential functional residues in human olfactory receptors.

Correlated mutation analysis and molecular models of olfactory receptors have provided evidence that residues in the transmembrane domains form a binding pocket for odor ligands. As an independent test of these results, we have calculated positive selection moments for the alpha-helical sixth transmembrane domain (TM6) of human olfactory receptors. The moments can be used to identify residues that have been preferentially affected by positive selection and are thus likely to interact with odor ligands. The results suggest that residue 622, which is commonly a serine or threonine, could form critical H-bonds. In some receptors a dual-serine subsite, formed by residues 622 and 625, could bind hydroxyl determinants on odor ligands. The potential importance of these residues is further supported by site-directed mutagenesis in the beta-adrenergic receptor. The findings should be of practical value for future physiological studies, binding assays, and site-directed mutagenesis.

Amino Acid Sequence↗

PubMed2006

Quasiclassical trajectories on a finite element density functional potential energy surface: The C++H2O reaction revisited.

A new method for the representation of potential energy surfaces (PESs) based on the p version of the finite element method is presented and applied to the PES of the [COH2]+ system in order to study the C++H2O-->[COH]++H reaction through the quasiclassical trajectory method. Benchmark ab initio computations have been performed on the most relevant stationary points of the PES through a procedure that incorporates basis set extrapolations, the contribution of the core correlation energy, and scalar relativistic corrections. The electronic structure method employed to compute the many points needed to construct the PES is a hybrid density functional approach of the B3LYP type with geometry-dependent parameters, which improves dramatically the performance with respect of the B3LYP method. The trajectory computations shed light on the behavior of the COH2+ complex formed in the collision. At a fixed relative translational energy of 0.62 eV, which corresponds to the crossed beam experiments [D. M. Sonnenfroh et al., J. Chem. Phys. 83, 3985 (1985)], the complex dissociates significantly into the reactants (37%). However, the behavior for a thermal sampling at T=300 K is significantly different because only 9% of the trajectories where capture occurs lead to dissociation into the reactants. The latter kind of behavior is coherent with the view that simple ion-molecule reactions proceed quite often at the capture rate provided it is corrected by the fraction of the electronic states which, being nearly degenerate for the reactants, become attractive at short distances. For both T=300 K and crossed beam conditions, the trajectory computations indicate that COH2+ is the critical intermediate, in agreement with a recent work [Y. Ishikawa et al., Chem. Phys. Lett. 370, 490 (2003)] and in contrast with the interpretation of the crossed beam experiments. Besides, virtually all trajectories generate COH++H (>99%), but a significant proportion of the isoformyl cation is formed with enough vibrational energy as to surmount the COH+-HCO+ isomerization barrier, about 37% at T=300 K.

Journal Article↗

PubMed2006

Regulatory processes affecting androgen receptor expression, stability, and function: potential targets to treat hormone-refractory prostate cancer.

Prostate cancer cells rely on androgen receptor (AR) for proliferation and survival. Therefore, curing prostate cancer will require elimination of AR. Although androgen is the natural ligand that activates AR, AR activity is also subject to regulation by growth factor/growth factor receptor-stimulated signaling pathways that control the cell cycle. Cell cycle regulatory proteins and protein kinases in signaling pathways affected by growth factors can lead to AR activation in the absence of androgen. While downstream signaling proteins such as cyclins, cyclin-dependent kinases (CDKs), and pRB can modulate AR activity, upstream signaling pathways involving protein kinases such as mitogen-activated protein kinases, protein kinase A, and protein kinase B/Akt can affect post-translational modification of AR to affect not only AR function but also AR stability. Calcium and calmodulin (CaM), essential for proliferation and viability of a number of cells, including prostate cancer cells, play an important role in AR expression, stability, and function. CaM affects AR partly by interacting directly with AR and partly by activating protein kinases such as Akt and DNA-PK that can phosphorylate AR. The ubiquitin/26S proteasome pathway responsible for timely destruction of cell cycle regulatory proteins whose levels impede cell cycle progression also induces AR expression by activating NF-kappaB, and promotes AR activity by participating in the assembly of an AR transcription complex. Maspin, a serine protease inhibitor that is known mostly for its role as a tumor suppressor can also regulate AR intracellular localization and function by competing with AR for binding to the chaperone protein Hsp90 and co-repressor HDAC1, respectively. This perspective reviews the experimental evidence implicating these diverse cellular processes in AR expression, stability, and/or function, and presents a rationale for disrupting these cellular processes as a viable option for the treatment of both the hormone-sensitive and the hormone-insensitive prostate cancer.

Calcium↗

PubMed1997

Application of color Doppler M-mode echocardiography in the assessment of ventricular diastolic function: potential for quantitative analysis.

Color Doppler M-mode echocardiography provides a spatiotemporal map of blood distribution (v(s,t)) within the heart, with a typical temporal resolution of 5 ms, a spatial resolution of 300 microns, and a velocity resolution of 3 cm/s. M-mode echocardiographic data can be obtained along a streamline from the mid-left atrium to the mid-left ventricle from either the apical transthoracic window or the basal transesophageal window. A key parameter of the color Doppler M-mode is the transmitral propagation velocity, the slope of the leading edge of the M-mode derived E-wave. This propagation velocity is significantly less than the velocities measured within the E-wave by pulsed Doppler echocardiography and appears to provide important independent information about left ventricular filling pressures and diastolic function. Furthermore, color M-mode velocities can be processed quantitatively by the Euler equation to yield estimates of the small (< 2 mmHg) pressure gradients between the base and apex during filling, the first time such gradients have been measured noninvasively.

Diastole↗

PubMed2000

Labeled neoglycoproteins and human lectins as diagnostic and potential functional markers in salivary glands of patients with Sjögren's syndrome.

OBJECTIVE: The profile of glycans and their recognition by endogenous receptors (lectins) are increasingly attributed to disease process. Monitoring this can provide information on the pathogenesis of Sjögren's syndrome (SS). Commonly, plant lectins are employed for phenomenological glycan mapping. To go beyond this approach restricted to binding of exogenous probes, new markers measure ligand properties of glycans to human (not plant) lectins and the presence of sugar receptors completing a protein-carbohydrate recognition system. Carrier-immobilized sugar epitopes (neoglycoproteins) and purified human lectins establish this innovative panel. METHODS: The host defence molecules mannan binding lectin, serum amyloid P component, and the macrophage migration inhibitory factor-binding sarcolectin, selected for their involvement in cell destructive mechanisms, were purified and labeled. The plant lectins SNA and MAA were employed to monitor regulation of potential ligand sites for I-type lectins and galectins. Asialofetuin was tested as a "pan-galectin selective" probe. The specific binding characteristics were determined by quantitative morphometry and statistical analysis. RESULTS: Diagnostic information emerged from this analysis. The percentage of stained tissue area was significantly different between SS and control specimens after processing with GlcNAc and Man-bearing neoglycoproteins and the 2 tested serum lectins. For separation of cases of primary and secondary SS, the staining intensity with the asialoglycoprotein, sarcolectin, and the exogenous alpha2,6-sialylated glycan-binding lectin SNA was statistically significant. CONCLUSION: Saccharide-presenting probes to measure the cellular capacity to bind glycan epitopes and human lectins as sensors for endogenous binding sites have proven to be useful as diagnostic tools. We suggest the differences we observed reflect aberrations from the normal cellular homeostasis with relevance for the pathogenesis of SS and its manifestation as a primary or secondary syndrome.

Binding Sites↗

PubMed2007

Multi drug resistance-dependent "vacuum cleaner" functionality potentially driven by the interactions between endocytosis, drug size and Pgp-like transporters surface density.

In cells, multi drug resistance (MDR) is associated with Pgp-like transporters expression extruding drugs from cellular membranes. MDR is efficiently generated with a relatively small fraction of membrane transporters. As the insertion of drugs into cellular membranes is widespread, there are no reasons why a drug should incorporate the membrane in the vicinity of a transporter. As a result a further elusive hypothesis is usually invoked: these transporters act like "vacuum cleaners" of drugs embedded in the membrane. Nonetheless, how these transporters attract drugs remains obscure. To clarify the "vacuum cleaner" notion, we suggest that during its residency time in cellular membranes, the lateral movement of drugs from their point of insertion to transporters is governed by Brownian's diffusion, which allows the drugs/transporters interaction. Taking into account the functionality of Pgp-like transporters, namely the extrusion of drugs from the plasma membrane inner leaflet, we characterize how the state of drug resistance is triggered involving: membrane endocytosis, drug physico-chemical properties and the surface density of Pgp-like transporters. In addition, the theory developed provides for the first time a theoretical proof of Lipinski's second rule with regard to drugs' size (or MW) selectivity on their permeation across cellular membranes.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2003

Untangling the functional potential of PSA-NCAM-expressing cells in CNS development and brain repair strategies.

Central nervous system (CNS) neural stem cells (NSCs), which are mostly defined by their ability to self-renew and to generate the three main cell lineages of the CNS, were isolated from discrete regions of the adult mammalian CNS including the subventricular zone (SVZ) of the lateral ventricle and the dentate gyrus in the hippocampus. At early stages of CNS cell fate determination, NSCs give rise to progenitors that express the polysialylated form of the neural cell adhesion molecule (PSA-NCAM). PSA-NCAM(+) cells persist in adult brain regions where neuronal plasticity and sustained formation of new neurons occur. PSA-NCAM has been shown to be involved in the regulation of CNS myelination as well as in changes of cell morphology that are necessary for motility, axonal guidance, synapse formation, and functional plasticity in the CNS. Although being preferentially committed to a restricted either glial or neuronal fate, cultured PSA-NCAM(plus) progenitors do preserve a relative degree of multipotentiality. Considering that PSA-NCAM(+) cells can be neatly used for brain repair purposes, there is much interest for studying signaling factors regulating their development. With this regard, it is noteworthy that neurotransmitters, which belong to the micro-environment of neural cells in vivo, regulate morphogenetic events preceding synaptogenesis such as cell proliferation, migration, differentiation and death. Consistently, several ionotropic but also G-protein-coupled neurotransmitter receptors were found to be expressed in CNS embryonic and postnatal progenitors. In the present review, we outlined the ins and outs of PSA-NCAM(plus) cells addressing to what extent our understanding of extrinsic and in particular neurotransmitter-mediated signaling in these CNS precursor cells might represent a new leading track to develop alternative strategies to stimulate brain repair.

Animals↗

PubMed2003

Known and potential functions for the SLP-76 adapter protein in regulating T-cell activation and development.

The hematopoietic adapter protein SLP-76 is a critical component of multiple biochemical signaling 'circuits' in T cells that integrate proximal signaling events initiated by ligation of the T-cell receptor (TCR) into more distal pathways. Given the important role ascribed to TCR signaling in directing the outcome of thymocyte selection, it seems likely that SLP-76 may also function in signaling pathways that ultimately impact the establishment of the peripheral T-cell repertoire. It is generally accepted that the peripheral T-cell repertoire is selected in large part during T-cell development in the thymus. Molecular interactions between the TCR and self-peptide/major histocompatibility complexes expressed on thymic stromal elements dictate the fate of developing thymocytes. Thymocyte survival and further maturation (positive selection) require an active signal delivered to the cell as a consequence of TCR ligation. This raises the intriguing question of how a thymocyte can, for a narrow window of developmental time, obtain responsiveness to self while maintaining tolerance to these same determinants upon export to the periphery. This article reviews the current literature describing SLP-76-dependent signaling pathways in mature T cells and developing thymocytes. A potential role for this critical signaling intermediate in integrating signals leading to positive and negative selection of the peripheral T-cell repertoire is also discussed.

Adaptor Proteins, Signal Transducing↗

PubMed1984

The functional potential of the rabbit fimbria.

The ability of the normal rabbit fimbria to retrieve eggs after progressive reduction of its mucosal surface was tested on 16 New Zealand white rabbits. Group 1 had a small fimbrial resection; group 2 had a large one. The resected tissue was weighed, and in both groups the contralateral fimbria (internal control) was cut and sutured without resection. Four weeks later the animals were mated, and 12 hours afterwards the ovulation sites on each ovary were counted and both tubes excised. In vivo observations of the transport of cumulus surrogates by the experimental fimbria were made before tubal excision in group 2 animals. The natural eggs retrieved by the fimbria were recovered by flushing the resected tubes with saline. The infundibulum and fimbria were cut from the ampulla and weighed to calculate the amount of fimbrial resection achieved. In group 1 the experimental side retrieved 82% of the eggs; in group 2 the experimental side retrieved 72%. In vivo observations revealed the presence of a spontaneously formed neofimbria that transported cumulus surrogates in a normal pattern and at a normal rate. The fimbria appeared dispensable, a fimbrialike structure formed spontaneously, the functional results were optimal, and the number of ovulation after surgery was unchanged. Some similarities can be observed in women.

Animals↗