thin vs WBbt:0004017

The leukocyte-produced 'toxic' proteins turned out to act, not through any toxic feature of the proteins themselves, but by activating destructive mechanisms that pre-exist within the target cell.

Despite being widespread in the environment and causing medical and agricultural harm, virtually nothing is known about the host factors important to facilitate their growth and development inside of host cells.

This should, of course, come as no surprise as it is hard to imagine any biological process in which the regulated movement of vesicles within the cells is not critical at some step.

In press), failed to accumulate the lysosomotropic fluorescent dye quinacrine within their vacuoles, mimicking the phenotype of wild-type cells treated with ammonium.

Thus, combination of QC and ABT-888 decreased mBCSCs growth by activating APC and inhibiting BER within the cells.

This indicates that not only was local proliferation within the SVZ and distant structures inhibited, but also that migration itself was reduced indirectly since there were less cells to migrate from the SVZ.

We found the sulfonylpiperazine, MMV020291, to be the most invasion-specific inhibitor, blocking successful merozoite internalisation within human RBCs and having no substantial effect on other stages of the cell cycle.

DTX and NIC were incorporated within a nanofiber (NF) system to prevent on-site recurrence by local release and re-sensitize the DTX-resistant cells.

We also found that chloroquine, quinacrine, vindoline, and catharanthine, each of which enhanced VLB cytotoxicity in CEM/VLB1K cells by 10- to 15-fold, similarly inhibited [125I]NASV labeling of P-gp.

Whether its platelet-derived growth factor (PDGF)-like product functionally activates its receptors within the cell or at the cell surface has potential implications in efforts to intervene with the v-sis-transformed phenotype.

To identify the receptor regions within the cytoplasmic domains necessary for transcriptional regulation, the receptors were transiently expressed in rat hepatoma cells.

Oligonucleotides with weak target site binding affinity or with only partial target site homology were ineffective at inducing mutations in the SV40 vectors within the COS cells.

First, site directed mutagenesis was used to identify a basic amino acid sequence motif within Wnt-1 protein that is required for this protein to accumulate on the cell surface.

Within the cell death/survival pathway, Akt and its downstream protein Bad play an important role in kainic acid (KA)-induced cell death.

Ornithine decarboxylase (a rate limiting enzyme in polyamine biosynthesis), and gamma-glutamylcysteine synthetase (a rate limiting enzyme in glutathione biosynthesis), the two building blocks of the main cellular thiol trypanothione, were overexpressed in some of the resistant isolates.

Verapamil, a calcium channel blocker, affects drug uptake by preventing its efflux and thereby accumulation within the cell.

These findings confirm the existence of polymorphic loci within the reduced critical region of Sicd2 that regulate the severity of seizure-induced cell death.

The need for quantitation within a distinct cell type is particularly important because transcription factors must be expressed in specific amounts to perform their functions properly.

The central role that mitochondria assume within cells is evidenced by the broad impact of mitochondrial diseases, caused by defects in either mitochondrial or nuclear genes encoding for mitochondrial proteins, on different organ systems.

Fatty acid oxidation (FAO), primarily known as β-oxidation, plays a crucial role in breaking down fatty acids within mitochondria and peroxisomes to produce cellular energy and preventing metabolic dysfunction.

The regulatory roles of two key enzymes within this cascade, GLS1 and argininosuccinate lyase (ASL), were specifically investigated and verified by cellular and in vivo experiments, including those using stress-promoted and naturally aged animals, combined with GLS1 and ASL knockdown, and multiple rounds of metabolite analysis.

Several observations support a model where, in response to stress and reduced nutrients, a metabolic pathway is activated within which AMPK and SIRT1 concordantly function to ensure an appropriate cellular response and adaptation to environmental modifications.

The field of proteomics which focuses on identifying the dynamic nature of the protein content expressed within a particular cell, tissue, or organism, has provided many insights into these disturbing disorders.

The combination of dexamethasone, 8-bromo-3'-5'-cyclic adenosine monophosphate, and isobutylmethylxanthine, referred to as DCI, has been reported to optimally induce cell differentiation in fetal lung explants and type II epithelial cells.

An ample body of data supports the role of S. mansoni-driven DP2-mediated activation of eosinophils as the source of LTC4 during infection, including: (i) HQL-79 and CAY10471 impaired systemic eosinophilia, drastically decreasing eosinophils within peritoneum and hepatic granulomas of infected animals in parallel to a reduction in cysteinyl leukotrienes levels; (ii) peritoneal eosinophils were identified as the only cells producing LTC4 in PGD2-mediated S. mansoni-induced infection; (iii) the magnitude of hepatic granulomatous eosinophilia positively correlates with S. mansoni-elicited hepatic content of cysteinyl leukotrienes, and (iv) isolated eosinophils from S. mansoni-induced hepatic granuloma synthesize LTC4 in vitro in a PGD2/DP2 dependent manner.

Clinical analysis revealed the upregulation of Tim-4 within the hepatic lesions of patients with AE, with its expression spatially localized to macrophage-enriched regions and functionally linked to extracellular inflammatory modulation.

Peptides can accumulate within cells of the central nerve ring and can elicit physiological effects when released to interact with receptors on adjoining cells.

The six toxins caused shrinkage and thinning of the intestinal cells, contraction of the intestine from the body wall, vacuolization, and degenerated appearance of the pinewood nematodes.

This requires a mechanism within the cell that leads to either basolateral or apical ATP release to regulate renal tubular function.

Aspartate and alanine aminotransferases (AST and ALT) levels were similar to those of the controls, within the accepted normal limits, before and after treatment denoting absence of hepatocellular injury.

It has also been proposed that cN-II, together with purine nucleoside phosphorylase and hypoxanthine-guanine phosphoribosyltransferase, constitutes the "oxypurine cycle", thus regulating intracellular phosphoribosyl pyrophosphate (PRPP) concentrations.

Metabolic co-operation between hepatocytes and hypoxanthine-guanine phosphoribosyltransferase-deficient V79 cells was quickly and continuously blocked by CSC over 27 h, whereas the phorbol ester induced a transient block.

Ornithine decarboxylase antizyme (OAZ), a prominent regulator of cell proliferation, DNA/RNA transformation and tumorigenesis, can bind to ornithine decarboxylase (ODC) and facilitate its degradation.

Within the context of this proposal, products of the EGF-homologous invertebrate genes noted above would participate in the transfer of information required for the specification of cell fate from the extracellular compartment to the cell interior.(ABSTRACT TRUNCATED AT 400 WORDS)

Netrin-1 and its receptors deleted in colorectal cancer (DCC) and neogenin are expressed within the developing visual system and have been implicated in mediating axon guidance and cell migration.

The results indicated that PMA at 10(-7) M causes within 30 min after treatment the phosphorylation of at least ten different proteins in both the HL-60 and R-94 cells.

A class of wound-induced genes was activated directly within neoblasts, including the Runx transcription factor-encoding runt-1 gene. runt-1 was required for specifying different cell types during regeneration, promoting heterogeneity in neoblasts near wounds.

MSC were embedded within a previously characterized thermoresponsive block copolymer worm gel that can induce stasis in human pluripotent stem cells (hPSC) and then co-cultured with MM cells.

Thus, the study outlines the signaling network of rBm33 induced inflammatory responses within the host immune cells.

Recombinant SER was expressed within insect cells using the baculovirus expression system and detected by each of the anti-SER antibodies as well as anti-phosphotyrosine antibodies.

The resistance to Heterodera glycines 1 (Rhg1) locus is widely used by soybean breeders to reduce yield loss caused by soybean cyst nematode (SCN). α-SNAP (α-soluble NSF attachment protein) within Rhg1 locus contributes to SCN resistance by modulation of cell status at the SCN feeding site; however, the underlying mechanism is largely unclear.

We demonstrate that the MiMSP8 protein is expressed in the dorsal gland of M. incognita juveniles and it can also be detected within giant cells induced by nematodes.

Histological analysis of nematode feeding sites indicated that WRKY45 was highly expressed within the feeding cells and associated vascular parenchyma cells.

The Meloidogyne incognita effector MiISE5 is exclusively expressed within the subventral esophageal cells and is upregulated during early parasitic stages.

Root-knot nematodes (RKNs, Meloidogyne spp.) are sedentary biotrophic pathogens that establish within the vascular cylinder of plant roots, forming a gall and inducing several feeding cells, giant cells (GCs), essential for completion of their life cycle.

When nematodes invade and subsequently migrate within plant roots, they generate cell wall fragments (in the form of oligogalacturonides; OGs) that can act as damage-associated molecular patterns and activate host defence responses.

Endoparasitic nematodes complete their life cycle within the root vascular cylinder, inducing specialized feeding cells: giant cells for root-knot nematodes and syncytia for cyst nematodes.

Cyst nematodes are devastating plant parasites that become sedentary within plant roots and induce the transformation of normal plant cells into elaborate feeding cells with the help of secreted effectors, the parasitism proteins.

Cyst nematodes induce specific syncytial feeding structures within the root which develop from an initial cell by successive incorporation of neighbouring cells through local cell wall dissolutions followed by hypertrophy of included cells.

Pratylenchus thornei are migratory nematodes that feed and reproduce within the wheat root cortex, causing cell death (lesions) resulting in severe yield reductions globally.

Plant endoparasitic nematodes, root-knot and cyst nematodes (RKNs and CNs) induce within the root vascular cylinder transfer cells used for nourishing, termed giant cells (GCs) and syncytia.

Cytosolic proteinases carry out a variety of regulatory functions by controlling protein levels and/or activities within cells.

The Fem1b gene is expressed in pancreatic islets, within both beta cells and non-beta cells, and is highly expressed in INS-1E cells, a pancreatic beta-cell line.

UidA (Gus) transcripts were detectable within giant-cells induced in tobacco roots at 11-13 days postinoculation with M. incognita as determined by in situ mRNA hybridization.

It inhabits plants and induces unique feeding site structures within host roots, known as giant cells (GCs).

MIR408 expression was located within nematode-induced feeding cells like its regulator SPL7 and was regulated by copper.

Within the Caenorhabditis elegans excretory cell, which forms an intracellular tube, the exocyst vesicle-tethering complex is enriched at the lumenal membrane and is required for its outgrowth, suggesting that exocyst-targeted vesicles extend the lumen.

Often, the response is triggered within cells, by detection of infection-induced damage, mainly in the intestine or epidermis.

Results showed that fucoxanthin at a concentration of 5 μM caused the most pronounced antioxidant effect in the late passage cells.

Urolithin A alleviated OGD/R-induced injury in N2a cells and neurons and reduced ischemic brain injury in mice.

Nuclei within cells are constantly subjected to compressive, tensile, and shear forces, which regulate nucleoskeletal and cytoskeletal remodeling, activate signaling pathways, and direct cell-fate decisions.

Urolithin A (Uro-A) activates mitophagy in mammal cells and Caenorhabditis elegans.

The zinc released within cells acts as a messenger in a signaling pathway to promote mobility acquisition.

Our results show that serine 204 within Smad3 is the key Pin1-binding site during inhibition of myoblast fusion and that both the transforming growth factor-β receptor and extracellular signal-regulated kinase (ERK)-mediated phosphorylation are required for the interaction of Pin1 with Smad3.

Reactive oxygen species (ROS) are highly reactive, oxygen-containing molecules that can cause molecular damage within the cell.

Our results therefore argue that EGFR can be regulated by allosteric changes within an existing receptor dimer--resembling signalling by insulin receptor family members, which share similar extracellular domain compositions but form covalent dimers.

The TZ/CIZE, potentially acting as a lipid gate, limits the abundance of the phosphoinositide PIP2 within cilia and is required for cell signalling.

Mutation of predicted phosphorylation sites within these motifs caused measurable loss of eff-1 gene function in cell fusion in vivo.

As an example discussed here, modulating latent stress response pathways within the cell provides exciting therapeutic potential, however, opposing views have emerged in the fields of degenerative disease and cancer.

One of the most significant achievements in biological science in the last decade is the discovery of RNA interference (RNAi), a process within living cells that regulates gene expression at post-transcriptional levels.

Herein, we show that Fem1b interacts with Gli1 within cells, and directly binds Gli1.

Tightly regulated pathways maintain the balance between proliferation and differentiation within stem cell populations.

These studies indicate that epigenetic mechanisms operating within the germ cell cycle of this organism filter and maintain an epigenetic memory that is required for germ cell function and can also influence gene expression in somatic lineages.

The accumulation of serpin oligomers and polymers within the endoplasmic reticulum (ER) causes cellular injury in patients with the classical form α1-antitrypsin deficiency (ATD).

New results indicate that epithelial defense in C. elegans can be triggered through detection of pathogen-induced perturbation of core physiology within host cells and through autophagic defense against intracellular and extracellular pathogens.

Ligand binding ultimately leads to gamma-secretase cleavage within the transmembrane domain, allowing the intracellular domain to translocate to the nucleus and activate target gene transcription.

Hs4F01 and its protein product were exclusively expressed within the dorsal oesophageal gland secretory cell in the parasitic stages of H. schachtii.

Amazingly, a single miRNA can regulate the expression of hundreds of mRNAs or proteins within a cell.

MicroRNAs (miRNAs) are tiny, endogenous nucleotides that bind to mRNA and induce translation repression within metazoan cells.

In contrast, we show that within the metazoan Caenorhabditis elegans, the heat shock response of somatic cells is not cell-autonomous but rather depends on the thermosensory neuron, AFD, which senses ambient temperature and regulates temperature-dependent behavior.

Our data support a model where CENP-A phosphorylation is involved in regulating Aurora B, INCENP, and PP1gamma1 targeting within the cell.

However, overexpression of NRBP caused a dramatic redistribution of the Golgi-associated marker p58 to more peripheral locations within the cell, consistent with an impairment of the ER to Golgi transport.

Furthermore, RNAi-induced gene silencing varies from minimal to complete loss-of-function phenotypes within homogeneous and between different cell populations.

The serine/threonine-specific phosphatase functions within a signal transduction pathway that regulates gene expression and biological responses in many developmentally important cell types.

We have identified and characterized a monoclonal antibody, F2-P3E3, that recognizes a Caenorhabditis elegans apoptotic epitope expressed within phagocytic cells, which is conserved in four other nematode species.

TnT is a muscle contractile protein that, in association with the thin filament proteins tropomyosin, troponin I and troponin C, regulates myosin-actin interaction in response to a rise in intracellular Ca2+.

These enzymes function within highly conserved modules of sequentially activating protein kinases that transduce signals from diverse extracellular stimuli.

Within 24 h, a significant proportion of green fluorescent protein-positive cells contained condensed chromatin, whereas vector-only controls remained viable.

TnT tethers troponin I (TnI) and troponin C (TnC) to the thin filament via tropomyosin (Tm), and TnT/Tm regulates the activation and inhibition of myosin-actin interaction in response to changes in intracellular [Ca2+].

TGF alpha plus TGF beta caused a significant decrease in bcl-2 mRNA levels within 3 h of treatment of T/I cells, followed by a progressive decline to 10% of control levels after 24 h of treatment.

The evidence accrued to date suggests that microwave radiation causes measurable stress to transgenic nematodes, presumably reflecting increased levels of protein damage within cells (the common signal thought to trigger hsp gene induction).

AMP-activated protein kinase (AMPK) is a key metabolic regulator which responds to changes in the AMP:ATP ratio within cells.

Astaxanthin is a marine xanthophyll carotenoid which effectively prevents intracellular oxidative stress and has beneficial effects against various human diseases.

The proteostasis network apparently functions within the cell, however, a myriad of studies indicate that this nexus of mechanisms is regulated at the organismal level by signaling pathways.

Moreover, GPA inhibited xanthine oxidase (XOD), glutamate dehydrogenase (GLDH), fatty acid synthase (FAS), phosphorylation of P38 MAPK, and upregulated the expression of SIRT3 and CPT1A protein production to control lipid metabolism and produce antioxidant benefits in cells and golden hamsters.

This allowed us to calculate mRNA half-lives within specific cell types and developmental stages and identify differentially regulated mRNA decay throughout embryonic development.

Functioning as a signaling hub within the cell, mitochondria integrate information from various intracellular compartments to regulate cellular signaling and metabolism.

These oligonucleotide therapeutics exert their efficacy by binding to target RNAs present within cells; however, the mechanisms underlying their cellular uptake, especially their passage through membranes, remain largely unclear.

The levels of ROS within the cell can be regulated by antioxidant enzymes, such as superoxide dismutase (SOD), which converts superoxide to hydrogen peroxide.

The flow of viscous fluid within the cytoplasm generates forces that re-arrange intracellular organelles, such as mitotic spindles and nuclei, to regulate cell growth, migration, and polarity.

Moreover, FTSB and ECH increase α-Syn fluidity within condensates, inhibit α-Syn transition into amyloid fibrils and reduce fibril-induced toxicity in SH-SY5Y cells.

Membrane trafficking is a conserved process required for the import, export, movement, and distribution of proteins and other macromolecules within cells.

This allows us to calculate mRNA half-lives within specific cell types and developmental stages, and identify differentially regulated mRNA decay throughout embryonic development.

Together, we reveal that the interplay between a kinase and RNA-binding proteins regulates the expression of lipid metabolism genes within neural cells, potentially impacting stress resistance and longevity.

Endocytosis is an essential process required for the movement of proteins and lipids within cells.

Membrane trafficking is a conserved process required for the movement and distribution of proteins and other macromolecules within cells.

In addition to scaffolding proteins that shape these mitotic chromosomes, post-translational modifications of histones within nucleosomes modulate chromosome dynamics throughout the cell cycle.

Such an effect of enhancing autophagic flux promotes both the cargo encapsulation within autophagosomes and degradation in autolysosomes in nearby cells.

Further, these proteins interact with other major regulatory factors, and any variations in their levels within the cell can alter the stoichiometry of these interactions, affecting diverse regulatory pathways.

In this study, we identify the cis-acting sequences within hlh-2prox and transcription factors required for the initial expression of hlh-2 in the α and β cells and their parents, demonstrate that the Wnt/β-catenin Asymmetry Pathway (WβA) regulates restriction of hlh-2 transcription to the α cells, and show that the maintenance of hlh-2 transcription in α cells requires distinct elements and the chromatin factor LSY-12.

Thus, in our experimental conditions, i.e., within 30-50 days post-N. brasiliensis infection, we observed an enhancement of the anorectic effect of exogenous CCK involving mast cell degranulation and histamine.

The broad range in cellular osmolarity within Zinnia mesophyll cell populations, coupled with inhibition of differentiation in the low range due to cell expansion and in the high range due to plasmolysis, may help explain why tracheary element differentiation in Zinnia suspension cultures is never complete nor perfectly synchronous and enable further optimization of this culture system.

The success of microbial endosymbionts, which reside naturally within a eukaryotic "host" organism, requires effective microbial interaction with, and manipulation of, the host cells.

The recently discovered class of tumour promoters, the teleocidins, are as potent as TPA in the induction of ornithine decarboxylase in mouse skin, the inhibition of differentiation of Friend erythroleukaemia cells, the induction of HL-60 cell adhesion and the promotion of tumours on mouse skin.

Ornithine decarboxylase (ODC), through the regulation of polyamine biosynthesis, influences normal mucosal growth and cell proliferation.

A functional LC3-interacting region motif within FAIM2 was essential for the interaction with LC3 and rescue of autophagy flux in shFAIM2 cells while LC3-binding property of FAIM2 was dispensable for the anti-apoptotic function in response to Fas receptor-mediated apoptosis.

Molecular docking suggested a putative binding area within c-Jun N-terminal kinase/extracellular signal-regulated kinase (JNK/Erk) protease active sites through the structural mimicking of adenosine phosphate (ANP) by the spatial combination of PL with ZA.

Though antiviral drugs with antioxidant properties confer potential abilities for preventing viral entry, those with pro-oxidant properties could induce the degradation of nascent viral RNA within the host cells, as RNAs are highly prone to ROS mediated degradation than DNA/proteins.

These results show that alpha-oligonucleotides can exhibit a sequence-specific antiviral effect and suggest that they may inhibit splicing reactions and be useful in targeting specific nucleic acid sequences within the cell nucleus.

We suggest that the functional coupling between SOCE and protein synthesis is likely to be critical for maintaining [Ca(2+)](ER) within a range that is required to prevent ER stress during changes in cellular translational activity.

These findings demonstrated that NAC could significantly influence gene expression within this pathway, thereby clarifying the exact relationship between the PI3K/Akt/mTOR signaling cascade and the underlying cellular processes controlling proliferation and apoptosis.

It has been suggested that copper-zinc superoxide dismutase (CuZn SOD) increment, by accelerating hydrogen peroxide formation, might promote oxidative damage within trisomy 21 cells and might be involved in the various neurobiological abnormalities found in Down's syndrome such as premature aging and Alzheimer-type neurological lesions.

Type VI collagen forms thin-beaded filaments that may interact with fibrils and cells.

The diverse gene expression changes occurring within the host cells suggest that both types of plant-parasitic nematodes modulate a variety of plant processes.

This secreted enzyme is produced in the nematode's esophageal glands and appears to function within the plant cell to manipulate the plant's shikimate pathway, which controls plant cell growth, development, structure, and pathogen defense.

This is most likely caused by an increase in antizyme-mediated degradation of ornithine decarboxylase-1 and a resulting reduction in cellular polyamine levels.

Given that receptor abundance or concentration within the plasma membrane plays key roles in determining signaling efficiency, these observations may point to a novel mechanism for modulating receptor-mediated cellular signaling.

These results suggest that, in addition to ER quality control, assembled AChRs are sorted within the Golgi system by a mechanism that controls the amount of cell-surface AChRs in a subtype-specific way.

Some PDZ-containing proteins are more dynamically regulated in distribution and may also be involved in the trafficking of interacting proteins within the cell.

It has been suggested that PC1/PC3 and PC2 are involved primarily in the processing of prohormones within the regulated secretory pathway of cells of endocrine and neural tissue.

Furthermore, the active compounds could completely inhibit the slimy substances and microbial cells on the surface of the squid and shrimp.

Additionally, we identified subpopulations within the fly crop that show circadian rhythm-regulated secretory properties and hypothesize an analogy between fly principal cells from different segments and distinct mouse kidney tubules.

Promoting mitophagy within cells could be a promising therapeutic strategy for delaying PFBS-induced aging.