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At least 577 records · Page 32Linked to original sources
PubMed1989

The interplay between platelet and vessel-wall mediators in coronary artery occlusion.

Myocardial infarction (MI) is associated with platelet aggregation and coronary vasospasm. Endogenous mediators produced by platelets and the vessel wall alter platelet function and smooth muscle tone and may be involved in the infarctive process. The synthesis and actions of these mediators is largely determined by interactions between platelets and the vessel-wall. MI occurs at sites of endothelial cell damage where the balance of mediators is shifted in favour of aggregation and vasospasm. Therapeutic intervention should aim at restoring the balance of mediators, and this will involve manipulation of endothelium-derived nitric oxide or its intracellular second messengers.

Biological Factors↗
PubMed1992

Interplay of steroid hormone receptors and transcription factors on the mouse mammary tumor virus promoter.

The mouse mammary tumor virus (MMTV) promoter, that responds to glucocorticoids and progestins, contains a complex hormone response element (HRE) in the long terminal repeat (LTR) region covered by a phased nucleosome. Hormone treatment leads to alterations in chromatin structure that make the HRE region more accessible to digestion by DNase I and permit binding of transcription factors, including nuclear factor I (NFI), immediately downstream of the HRE. NFI acts as a basal transcription factor on the MMTV promoter in vitro but competes with the hormone receptors in terms of binding to free DNA. In uninduced chromatin, the precise positioning of the DNA double helix on the surface of the histone octamer precludes binding of NFI to its cognate sequence while still allowing recognition of the HRE by the hormone receptors. We postulate that receptor binding to the nucleosomally organized MMTV promoter disrupts the chromatin structure enabling NFI binding and subsequent formation of a stable transcription complex. Whether the receptor remains bound to DNA during induction or is displaced by NFI is not conclusively known, but our evidence supports a "hit and run" mechanism. NFI is not the only factor involved in hormonally induced transcription of the MMTV promoter. Two degenerated octamer motifs located immediately upstream of the TATA box are recognized by the ubiquitous transcription factor OTF-1 (Oct-1, NFIII), and are also important. In vitro, mutations in these motifs do not influence basal transcription, but completely abolish the stimulatory effect of purified progesterone receptor. Progesterone receptor bound to the HRE facilitates binding of OTF-1 to the two octamer motifs. Thus, OTF-1 is a natural mediator of progesterone induction of the MMTV promoter and acts through cooperation with the hormone receptor for binding to DNA.

Animals↗
PubMed1993

Cdc2 activation: the interplay of cyclin binding and Thr161 phosphorylation.

The mitotic kinase cdc2 must bind to a regulatory subunit--a cyclin--to be active. Cyclin binding controls the timing of activation of the kinase subunit, by modulating its interaction with upstream regulatory enzymes, and it also determines subcellular localization and substrate specificity. In this article, I summarize our present knowledge of the mechanisms that control cdc2 activation.

Journal Article↗
PubMed2005

Divergent evolution in the enolase superfamily: the interplay of mechanism and specificity.

The members of the mechanistically diverse enolase superfamily catalyze different overall reactions. Each shares a partial reaction in which an active site base abstracts the alpha-proton of the carboxylate substrate to generate an enolate anion intermediate that is stabilized by coordination to the essential Mg(2+) ion; the intermediates are then directed to different products in the different active sites. In this minireview, our current understanding of structure/function relationships in the divergent members of the superfamily is reviewed, and the use of this knowledge for our future studies is proposed.

Amino Acid Sequence↗
PubMed2004

Substance use and posttraumatic stress disorders: symptom interplay and effects on outcome.

This study examined concurrent and prospective associations between substance use disorder (SUD) and posttraumatic stress disorder (PTSD) diagnosis and symptoms and mechanisms underlying these associations. Participants (n = 133) were assessed at intake and 6 months following inpatient SUD treatment. Patients differed by baseline PTSD status on psychiatric comorbidity and substance use history but not on current substance use symptoms. Participants with alcohol use disorders reported a greater number of reexperiencing symptoms. Baseline PTSD status did not predict substance use outcome. However, change in PTSD status over follow-up predicted substance use outcomes; those with unremitted PTSD demonstrated poorer SUD outcome than those with remitted PTSD. General psychiatric distress at follow-up was associated with poorer outcomes, and such distress mediated the association between PTSD change status and substance use outcome. Findings suggest that clinicians should assess for PTSD among those with SUD and, during treatment, should monitor PTSD and other psychological symptoms, which may be risk factors for relapse to substance abuse.

Adolescent↗
PubMed2005

Separation-individuation revisited: on the interplay of parent-adolescent relations, identity and emotional adjustment in adolescence.

The objective of this study was to test our alternative interpretation of the separation-individuation hypothesis. This interpretation states that separation from the parents is not a precondition for individuation, but rather separation and individuation are two parallel processes of development during adolescence. We investigated our interpretation in two ways. Firstly, we looked at descriptive age differences in parental support and development of relational and societal identity. Secondly, we investigated the variation with age of the associations between parental support and emotional adjustment, and identity and emotional adjustment. Data of a representative Dutch sample of 2814 adolescents, aged 12-24 were used. In both cases, the findings supported our interpretation of the separation-individuation hypothesis and similar results were found in the descriptive analyses and the structural equation models. Parental support decreased with age, and so too did its association with emotional adjustment. In other words, as adolescents become older, they experience less parental support, while its importance for their emotional adjustment also declines. The opposite pattern was observed with respect to identity development: as adolescents become older, their relational and societal identity commitments develop, and the degree to which these commitments are developed also becomes more important for their emotional adjustment.

Adaptation, Psychological↗
PubMed2006

The interplay between antiviral activity, oligonucleotide hybridisation and nucleic acids incorporation studies.

Nucleoside analogues have been the most successful antiviral compounds. Likewise, they are the most intriguing antiviral compounds, because of their structural relationship to natural nucleosides. This is also the reason why the design process of a potential selective antiviral nucleoside is so difficult. Too many natural processes (from cellular uptake to DNA incorporation) and too many enzymes are involved in their biological effect (activity/toxicity/catabolism/anabolism) to make the design process readily predictable. The relationship between the physicochemical and biochemical properties of nucleoside analogues and their antiviral activity is very complex and could only be understood on a very long term basis. Here we try to explain some of the reasoning that was made during the design process leading to new potent antivirals with a phosphonate functionality.

Anti-HIV Agents↗
PubMed2004

The interplay between the Bcl-2 family and death receptor-mediated apoptosis.

Two principal pathways for apoptosis initiation exist. One pathway, which is also termed the 'extrinsic' pathway, is mediated by death receptors, a subgroup of the TNF receptor superfamily. The second pathway, which is also referred to as the 'intrinsic' pathway is controlled by members of the Bcl-2 family. A long standing discussion revolves around the question of how these two pathways influence each other in regulating the decision about life or death of a cell. Here, we review our current knowledge about the interactions between these two pathways and discuss current models which could help to resolve previous apparently contradictory results.

Animals↗
PubMed2006

Interplay between PI3K/Akt and MAPK signaling pathways in DNA-damaging drug-induced apoptosis.

In order to elucidate the role of the mitogen-activated protein kinases, including JNK, p38 MAPK and ERK, as well as the survival-associated PI3K/Akt signaling pathway, in the response to chemotherapy, we have conducted a comparative study regarding the effects of doxorubicin on these pathways. Doxorubicin was determined to elicit the apoptosis of NIH3T3 cells in a dose-dependent manner. Prior to cell death, both Akt and p38 MAPK were transiently activated, and subsequently inactivated almost wholly, whereas ERK and JNK evidenced sustained activations in response to the drug treatment. The inhibition of PI3K/Akt and p38 MAPK both accelerated and enhanced doxorubicin-induced apoptosis and ERK inhibition apparently exerted negative effect on apoptosis. The modulation of PI3K/Akt activation by treatment of LY294002 or expression of Akt mutants such as Akt-DN or Myr-Akt exerted a significant effect on the activation of ERK1/2. We also observed that PI3K/Akt and sustained ERK activation were associated intimately with the etoposide-induced apoptosis. Taken together, our results clearly suggest that the differential regulation of the PI3K/Akt, ERK1/2, and p38 MAPK signaling pathways are crucial in the context of DNA-damaging drug-induced apoptosis, and this has compelled us to propose that the sustained activation of ERK1/2 pathway may be generally involved in the apoptosis induced by anticancer DNA-damaging drugs, including doxorubicin and etoposide.

Animals↗
PubMed2006

Import of peroxisomal membrane proteins: the interplay of Pex3p- and Pex19p-mediated interactions.

In contrast to the molecular mechanisms underlying import of peroxisomal matrix proteins, those involving the transport of membrane proteins remain rather elusive. At present, two targeting routes for peroxisomal membrane proteins (PMPs) have been depicted: class I PMPs are targeted from the cytoplasm directly to the peroxisome membrane, and class II PMPs are sorted indirectly to peroxisomes via the endoplasmic reticulum (ER). In addition, three peroxins--Pex3p, Pex16p, and Pex19p - have been identified as essential factors for PMP assembly in several species including humans: Pex19p is a predominantly cytoplasmic protein that shows a broad PMP-binding specificity; Pex3p serves as the membrane-anchoring site for Pex19p; and Pex16p - a protein absent in most yeasts--is thought to provide the initial scaffold for recruiting the protein import machinery required for peroxisome membrane biogenesis. Remarkably, the function of Pex16p does not appear to be conserved between different species. In addition, significant disagreement exists about whether Pex19p has a chaperone-like role in the cytosol or at the peroxisome membrane and/or functions as a cycling import receptor for newly synthesized PMPs. Here we review the recent progress made in our understanding of the role of two key players in PMP biogenesis, Pex3p and Pex19p.

Endoplasmic Reticulum↗
PubMed2003

Functional interplay between modulation of histone deacetylase activity and its regulatory role in G2-M transition.

The acetylation status of histones plays an essential role in regulating transcription and replication, and is thus involved in the proliferation and differentiation of normal and neoplastic cells. Here, we investigated the effect of trichostatin A (TSA), an inhibitor of histone deacetylases (HDACs), on G2-M transition during the cell cycle. HDAC inhibition by TSA arrested the cell cycle at G2 and also induced escape from the mitotic arrest into G1. TSA reduced the expression of cyclin B1, a key cyclin for G2-M transition, but stimulated expression of p21(WAF1/Cip1), an inhibitor of CDK and Cdc2. In contrast, the expression of cyclin B1 but not p21(WAF1/Cip1) is enhanced during M. Moreover, histone acetylation at promoters of these two genes was regulated by TSA. TSA augmented acetylation of the p21(WAF1/Cip1) promoter but reduced that of the cyclin B1 promoter, suggesting the relationship between TSA-induced modulation of histone acetylation and differential expression of these genes. Taken together, our observations suggest that modulation of HDAC activity is implicated in the G2-M transition by regulating the transcription of cell cycle regulators, p21(WAF1/Cip1) and cyclin B1, via modulating acetylation status of the histones at their promoters.

Cell Line↗
PubMed2005

Interplay between the cis-prenyltransferases and polyprenol reductase in the yeast Saccharomyces cerevisiae.

Dolichol formation is examined in three Saccharomyces cerevisiae strains with mutations in the ERG20 gene encoding farnesyl diphosphate synthase (mevalonic acid pathway) and/or the ERG9 gene encoding squalene synthase (sterol synthesis pathway) differing in the amount and chain length of the polyisoprenoids synthesized. Our results suggest that the activities of two yeast cis-prenyltransferases Rer2p and Srt1p and polyprenol reductase are not co-regulated and that reductase may be the rate-limiting enzyme in dolichol synthesis if the amount of polyisoprenoids synthesized exceeds a certain level. We demonstrate that reductase preferentially acts on typical polyprenols with 13-18 isoprene residues but can reduce much longer polyprenols with even 32 isoprene residues.

Alkyl and Aryl Transferases↗
PubMed2005

Evaluation of polydimethylsiloxane scaffolds with physiologically-relevant elastic moduli: interplay of substrate mechanics and surface chemistry effects on vascular smooth muscle cell response.

Polydimethylsiloxane (PDMS) is used extensively to study cell-substrate interactions because its mechanical properties are easily tuned in physiologically relevant ranges. However, changes in mechanical properties also modulate surface chemistry and cell response. Here, we correlate the mechanical and surface properties of PDMS to vascular smooth muscle cell (VSMC) behavior. We find that a 5-fold increase in base:crosslinker ratio leads to approximately 40-fold decrease in elastic modulus but no significant differences in surface wettability. However, when polyelectrolyte multilayers are adsorbed to promote cell adhesion, wettability varies inversely with substrate stiffness. Despite these differences in hydrophobicity, the amount of adsorbed protein remains the same. In the absence of serum, there is a 39% decrease in cell attachment and a 42% decrease in spreading as the elastic modulus decreases from 1.79 to 0.05 MPa. In the presence of serum or adsorbed fibronectin, the differences in attachment and spreading are diminished. This is not the case for the rate of serum-stimulated cell proliferation, which remains inversely dependent on crosslinker concentration. We conclude that for the range of crosslinker concentrations investigated, the surface properties dominate the initial cell attachment and spreading, whereas the mechanical properties influence the long-term cell growth.

Adsorption↗
PubMed2006

Successful antidepressant therapy restores the disturbed interplay between TNF-alpha system and HPA axis.

BACKGROUND: In depressed patients, alterations in the hypothalamo-pituitary-adrenocortical (HPA) system are the most consistent neurobiological finding. HPA axis activity and cytokines are intrinsically intertwined: inflammatory cytokines stimulate adrenocorticotropic hormone (ACTH) and cortisol secretion, while, in turn, glucocorticoids suppress the synthesis of proinflammatory cytokines. METHODS: We examined alterations in plasma levels of tumor necrosis factor-alpha (TNF-alpha), levels of its soluble receptors p55 (sTNF-R p55) and p75 (sTNF-R p75) as well as changes in the HPA system function using the combined dexamethasone/corticotropin-releasing hormone (dex/CRH) test on admission and at discharge in 70 depressed inpatients without inflammation. RESULTS: On admission, TNF-alpha levels were inversely associated with the ACTH response to the combined dex/CRH test. Changes in TNF-alpha, sTNF-R p55, and sTNF-R p75 plasma levels from admission to discharge were positively correlated with the dex/CRH test outcome at discharge. Subgroup analysis revealed that this association was restricted to those patients achieving remission. In this subgroup, TNF-alpha levels at discharge were also positively correlated with dex/CRH test response at discharge. CONCLUSIONS: Our results suggest that elevated HPA axis activity in acute depression suppresses TNF-alpha system activity, while after remission, when HPA axis activity has normalized, the TNF-alpha system seems to gain influence on the HPA system.

Adult↗