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Results for “Integrative interaction”

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PubMed1991

[Cardiovascular risk factors--an integrated sympathetic viewpoint].

A large body of experimental and clinical data concerning the "classical cardiovascular risk factors" may be integrated into a unifying concept in which an increase in sympathetic activity and nutritional factors play a crucial role. The enhancement of sympathetic activity (e.g. as a consequence of psychosocial stress), induces--via direct and indirect mechanisms--activation of the renin-angiotensin-aldosterone system and the insulin axis. Balanced endothelial function may also be disrupted. Subsequently, these alterations lead to cardiovascular remodelling and development of the early stages of arteriosclerosis. Mechanical forces such as pressure and strain, and also mild hyperinsulinemia with secondary elevations in the LDL/HDL ratio further amplify these processes. Wrong nutrition, characterized by an elevated salt, sugar and fat intake, further stimulates these pathological events. The chain of events finally leading to the clinical manifestation of arteriosclerosis is certainly strongly based on, and modified by, a genetic predisposition. Cigarette smoking acts as a pulsatile, exogenous amplifier of the sympathetic nervous system. Furthermore, complex interactions of the various "hormonal risk systems", namely renin-angiotensin, insulin, and LDL/HDL cholesterol, have been observed at the cellular and molecular level. These interactions are integratively influenced by environmental and sympathetic factors. Therefore, a comprehensive approach should be incorporated into prophylactic and therapeutic strategies.

Cardiovascular Diseases↗

PubMed1988

Molecular dynamics in the membranes of helper T cells.

We provide evidence that redistributions and interactions of integral proteins in the fluid membranes of helper T (Th) cells may play important roles in Th-cell activation. A particular monoclonal antibody, 3D3, directed to a clonotypic determinant on the T-cell receptor (TCR) of the cloned Th-cell line D10, had previously been shown to be distinctively capable of directly activating D10 cells at low concentrations. We demonstrate here by immunofluorescence experiments that it is also distinctively able itself to produce a clustering (capping) of the TCRs on the D10 cell surface. Simultaneously, by means of double-immunofluorescence experiments, we find that the 3D3-induced clustering of the TCRs distinctively produces a co-clustering of the accessory molecule CD4 with the TCR clusters, although the CD4 and TCR molecules are normally independent of one another in the D10 cell membrane. These results, and related ones previously obtained from studies of the interactions of D10 Th cells with antigen-presenting cells, are analyzed to suggest that the membrane clustering of TCRs and the induced TCR-CD4 interactions are critical to the signaling events in Th-cell activation.

Antibodies, Monoclonal↗

PubMed2025

Integration of multiple omics reveals key targets and cellular mechanisms for intervention in sarcopenia.

BACKGROUND: Sarcopenia, an age-related syndrome characterized by progressive loss of muscle mass, strength, and function, presents a significant global health burden with limited therapeutic interventions. This study integrates genomic causality, multi-tissue omics, and cellular mediation analyses to identify and prioritize mechanistically grounded therapeutic targets. METHODS: A multi-tiered analytical framework was applied, beginning with two-sample Mendelian randomization (MR) to infer causal relationships between 4907 plasma proteins (cis-pQTLs from 35,559 individuals) and sarcopenia traits in Pan-UK Biobank participants. Bayesian colocalization and transcriptomic validation in human sarcopenia muscle biopsies were employed to prioritize targets. Cellular mediation analysis quantified contributions of immune and stromal cell subtypes to protein-trait pathways using transcriptomic deconvolution. RESULTS: MR identified 1237 plasma proteins causally associated with sarcopenia traits, with six targets (HGFAC, GATM, HMOX2, F2, LMAN2L, HPGDS) validated through colocalization, transcriptomic expression, and sarcopenia-related dysregulation. Cellular mediation revealed immune mechanisms underlying HGFAC's effects, with CD4+ regulatory T cells mediating 3.49 % of its impact on sarcopenia traits. Prothrombin exhibited muscle-protective effects independent of coagulation. CONCLUSION: This study establishes a causal map linking plasma proteins to sarcopenia through immune-stromal interactions. The integration of MR, multi-omics validation, and cellular mediation prioritizes six proteins as actionable targets, supporting repurposing of thrombin inhibitors and development of immunometabolic therapies. The framework bridges genomic causality with cellular pathophysiology, advancing precision strategies for age-related muscle decline.

Humans↗

PubMed1998

Linking primary care performance to outcomes of care.

BACKGROUND: Substantial research links many of the defining characteristics of primary care to important outcomes; yet little is known about the relative importance of each characteristic, and several characteristics have not been examined. These analyses evaluate the relationship between seven defining elements of primary care (accessibility, continuity, comprehensiveness, integration, clinical interaction, interpersonal treatment, and trust) and three outcomes (adherence to physician's advice, patient satisfaction, and improved health status). METHODS: Data were derived from a cross-sectional observational study of adults employed by the Commonwealth of Massachusetts (N = 7204). All patients completed a validated questionnaire, the Primary Care Assessment Survey. Regression methods were used to examine the association between each primary care characteristic (11 summary scales measuring 7 elements of care) and each outcome. RESULTS: Physicians' comprehensive ("whole person") knowledge of patients and patients' trust in their physician were the variables most strongly associated with adherence, and trust was the variable most strongly associated with patients' satisfaction with their physician. With other factors equal, adherence rates were 2.6 times higher among patients with whole-person knowledge scores in the 95th percentile compared with the 5th percentile (44.0% adherence vs 16.8% adherence, P < .001). The likelihood of complete satisfaction was 87.5% for those with 95th percentile trust scores compared with 0.4% for patients with 5th percentile trust scores (P < .001). The leading correlates of self-reported health improvements were integration of care, thoroughness of physical examinations, communication, comprehensive knowledge of patients, and trust (P < .001). CONCLUSIONS: Patients' trust in their physician and physicians' knowledge of patients are leading correlates of three important outcomes of care. The results are noteworthy in the context of pervasive changes in our nation's health care system that are widely viewed as threatening to the quality of physician-patient relationships.

Adult↗

PubMed2001

Bitter substances suppress afferent responses to an appetitive mixture: evidence for peripheral integration of chemosensory stimuli.

The processes that lead from detection of chemicals, transduction, and coding with the appropriate message to initiate ingestion of a palatable meal or to reject a potentially noxious substance are poorly understood in vertebrates owing to the complex organization of the taste system. As a first step in elucidating the cellular basis of the behavioral differences elicited by appetitive stimuli and bitter compounds, we recorded from the afferent nerves conveying peripheral chemosensory information to the CNS in the head of the leech, Hirudo medicinalis. Superfusion of the chemosensory region of the lip of Hirudo with a mixture of NaCl (150 mM) and arginine (1 mM), an appetitive solution that elicits ingestion, increased the neuronal activity in the afferent cephalic nerves, for example (Zhang X, Wilson RJ, Li Y, Kleinhaus AL. 2000. Chemical and thermal stimuli have short-lived effects on the Retzius cell in the medicinal leech. J Neurobiol 43:304-311.). In the present paper we show that superfusing the lip with quinine or denatonium reduced the basal neural activity in the afferents. Furthermore, these bitter substances in the appetitive solution counteracted the increased activity the appetitive solution evoked in the cephalic nerves. Thus, the neural activity evoked by the application of appetitive and aversive stimuli to the chemosensory area of the lip paralleled the opposite behavioral responses to the same chemicals. The results suggest that individual leech taste cells possess receptors for both types of stimuli. Therefore, the leech may be a good model system in which to study peripheral taste events in cells that may possess multiple receptors and transduction mechanisms that interact to integrate information.

Action Potentials↗

PubMed1998

Linking multiple heterogeneous data sources to practice guidelines.

The BiliLIGHT system is a World Wide Web (Web) based system that integrates an interactive clinical practice guideline with real-time patient-data retrieval from remote heterogeneous data sources to help clinicians manage newborn jaundice at the point of care in three clinical settings. We briefly describe the system, how actual information exchange of medical data across institutional boundaries was achieved, and how the data were connected to a CPG. In particular, we examine the requirements for patient identification, exchange protocols, authentication, and a standard vocabulary.

Computer Systems↗

PubMed2025

Integration of multi-source gene interaction networks and omics data with graph attention networks to identify novel disease genes.

MOTIVATION: The pathogenesis of diseases is closely associated with genes, and the discovery of disease genes holds significant importance for understanding disease mechanisms and designing targeted therapeutics. However, biological validation of all genes for diseases is expensive and challenging. RESULTS: In this study, we propose DGP-AMIO, a computational method based on graph attention networks, to rank all unknown genes and identify potential novel disease genes by integrating multi-omics and gene interaction networks from multiple data sources. DGP-AMIO outperforms other methods significantly on 20 disease datasets, with an average AUROC and AUPR exceeding 0.9. The superior performance of DGP-AMIO is attributed to the integration of multiomics and gene interaction networks from multiple databases, as well as triGAT, a proposed GAT-based method that enables precise identification of disease genes in directed gene networks. Enrichment analysis conducted on the top 100 genes predicted by DGP-AMIO and literature research revealed that a majority of enriched GO terms, KEGG pathways and top genes were associated with diseases supported by relevant studies. We believe that our method can serve as an effective tool for identifying disease genes and guiding subsequent experimental validation efforts. AVAILABILITY AND IMPLEMENTATION: DGP-AMIO is publicly available at https://github.com/yangkaiyuan1027/DGP-AMIO.

Gene Regulatory Networks↗

PubMed2006

Multilocus analyses of Renin-Angiotensin-aldosterone system gene variants on blood pressure at rest and during behavioral stress in young normotensive subjects.

The renin-angiotensin-aldosterone system (RAAS) is a proteolytic cascade that regulates and maintains blood pressure (BP). This study aimed to explore the interactive and integrative effects of multiple RAAS polymorphisms on BP at rest and during behavioral stress in a normotensive population. A total of 920 young white and black twins (age: 12 to 30 years; 45% blacks) was subjected to three 10-minute stress tasks. Thirteen potential functional polymorphisms from 4 major RAAS genes were genotyped. We performed multilocus prediction allowing for genetic modification effects (gene-gene, gene-gender, gene-ethnicity, and gene-body mass index) using Multivariate Adaptive Regression Splines and generalized estimating equations. Single polymorphism analyses showed modest effects of M235T (angiotensinogen) and A-239T (angiotensin I-converting enzyme; P value range: 0.005 to 0.036), accounting for approximately 1% of the total variance of systolic BP at rest and during stress. Compared with this, the best multilocus models revealed multiple independent genetic modification effects (gene-gene, gene-gender, and gene-body mass index; P value range: 0.003 to 0.009), accounting for 2.5% and 7.3% of the total variance for systolic BP levels at rest and during stress, respectively. Our data support the hypothesis that multiple RAAS genetic modifications account for BP variation. We conclude that the RAAS genetic modifications may contribute more to the dynamic BP regulation in response to behavioral stress compared with the static BP value. In addition, we reported a gene-gene interaction between M235T (angiotensinogen) and A1159G (angiotensin I-converting enzyme) on stress systolic BP levels. We proposed a viable approach to test for the multiple genetic contributions to BP and hypertension.

Adolescent↗

PubMed1990

Kinetics of phosphorylation of Na+/K(+)-ATPase by protein kinase C.

The kinetics of phosphorylation of an integral membrane enzyme, Na+/K(+)-ATPase, by calcium- and phospholipid-dependent protein kinase C (PKC) were characterized in vitro. The phosphorylation by PKC occurred on the catalytic alpha-subunit of Na+/K(+)-ATPase in preparations of purified enzyme from dog kidney and duck salt-gland and in preparations of duck salt-gland microsomes. The phosphorylation required calcium (Ka approximately 1.0 microM) and was stimulated by tumor-promoting phorbol ester (12-O-tetradecanoylphorbol 13-acetate) in the presence of a low concentration of calcium (0.1 microM). PKC phosphorylation of Na+/K(+)-ATPase was rapid and plateaued within 30 min. The apparent Km of PKC for Na+/K(+)-ATPase as a substrate was 0.5 microM for dog kidney enzyme and 0.3 microM for duck salt-gland enzyme. Apparent substrate inhibition of PKC activity was observed at concentrations of purified salt-gland Na+/K(+)-ATPase greater than 1.0 microM. Phosphorylation of purified kidney and salt-gland Na+/K+ ATPases occurred at both serine and threonine residues. The 32P-phosphopeptide pattern on 15% sodium dodecyl sulfate-polyacrylamide gel electrophoresis after hydroxylamine cleavage of pure 32P-phosphorylated alpha subunit was the same for the two sources of enzyme, which suggests that the phosphorylation sites are similar. The results indicate that Na+/K(+)-ATPase may serve as a substrate for PKC phosphorylation in intact cells and that the Na+/K(+)-ATPase could be a useful in vitro model substrate for PKC interaction with integral membrane proteins.

Animals↗

PubMed2026

Programmed ribosomal frameshifting triggers translational stress to promote viral replication.

Programmed ribosomal frameshifting (PRF) is a conserved viral strategy for expressing polyproteins from compact genomes. Although PRF is traditionally viewed as a structural mechanism, here we show that it functions as a regulatory signal that rewires host translation in favor of viral replication. A minimal SARS-CoV-2 PRF element is sufficient to activate the GCN2 arm of the integrated stress response (ISR) independently of the canonical ISR sensor ZAKα. This activation serves as a temporal switch during early infection to shut off host translation and is required for viral propagation in cells and human airway organoids. Proteomic and genetic screens identify DRG1 and IGF2BP3 as key mediators of PRF-induced GCN2 activation. We further show that this PRF-GCN2 axis is conserved in human immunodeficiency virus (HIV)-1 and West Nile virus, highlighting its broad relevance across RNA viruses. These findings reveal a sophisticated mechanism of viral translational control, highlighting PRF as a stress-inducing module that enhances viral replication.

RNA virus↗

PubMed1996

A new taste reactivity analysis of the integration of taste and physiological state information.

We used conjoint manipulation of taste and physiological state to address the theoretical issue of signal integration. The interaction between taste (glucose concentration) and state (food deprivation) was evaluated using the taste reactivity method in which oral motor responses elicited by direct intraoral infusion are measured. The time frame of the typical taste reactivity paradigm, where observation is limited to the infusion period, was expanded to include the postinfusion interval. In each test session, rats received a series of trials consisting of 15-s intraoral infusions and 45-s postinfusion observation intervals. Two experiments were run in which glucose concentration was varied and rats were run nondeprived and after 24 h food deprivation. In experiment 1, glucose concentrations (0, 3.2, 6.25, 12.5, and 25%) were randomly presented during each test session. In experiment 2, individual glucose concentrations (0, 6.25, or 25%) were presented during separate sessions. For both, a deprivation condition was flanked by nondeprived (baseline) sessions. Concentration-response functions were comparable in both experiments. In each experiment, the shape of the concentration-response function was dramatically different during and after infusions. During infusions, there were no increases in glucose-elicited rhythmic oral responses beyond a very dilute concentration. After infusions, the concentration-response functions appeared linear across the concentration range. In both experiments, deprivation elevated responding only in the after-infusion periods. In experiment 1, the concentration-response function was uniformly elevated (on average, 27%) by deprivation, which if taken at face value would suggest an additive combination of taste and state feedback signals. In experiment 2, however, deprivation increased responding (approximately 30%) for 6.25%, but not for 0 or 25%, suggesting a stimulus specificity of the taste-state integration. Clearly then, the taste-state profiles differed as a function of experimental design. In the GENERAL DISCUSSION, we suggest that the uniform elevation of responding to all glucose concentrations, and to water, seen in experiment 1, may be an artifact of the random presentation of all stimuli during individual sessions. Experiment 2, in which stimuli were presented in a between-sessions design, may provide a truer reflection of the underlying integrative process.

Animals↗

PubMed2024

Neuronal differentiation requires BRAT1 complex to remove REST from chromatin.

Repressor element-1 silencing transcription factor (REST) is required for the formation of mature neurons. REST dysregulation underlies a key mechanism of neurodegeneration associated with neurological disorders. However, the mechanisms leading to alterations of REST-mediated silencing of key neurogenesis genes are not known. Here, we show that BRCA1 Associated ATM Activator 1 (BRAT1), a gene linked to neurodegenerative diseases, is required for the activation of REST-responsive genes during neuronal differentiation. We find that INTS11 and INTS9 subunits of Integrator complex interact with BRAT1 as a distinct trimeric complex to activate critical neuronal genes during differentiation. BRAT1 depletion results in persistence of REST residence on critical neuronal genes disrupting the differentiation of NT2 cells into astrocytes and neuronal cells. We identified BRAT1 and INTS11 co-occupying the promoter region of these genes and pinpoint a role for BRAT1 in recruiting INTS11 to their promoters. Disease-causing mutations in BRAT1 diminish its association with INTS11/INTS9, linking the manifestation of disease phenotypes with a defect in transcriptional activation of key neuronal genes by BRAT1/INTS11/INTS9 complex. Finally, loss of Brat1 in mouse embryonic stem cells leads to a defect in neuronal differentiation assay. Importantly, while reconstitution with wild-type BRAT1 restores neuronal differentiation, the addition of a BRAT1 mutant is unable to associate with INTS11/INTS9 and fails to rescue the neuronal phenotype. Taken together, our study highlights the importance of BRAT1 association with INTS11 and INTS9 in the development of the nervous system.

Humans↗

PubMed1983

Consultation-Liaison outcome evaluation system. I. Consultant-consultee interaction.

The Consultation-Liaison Outcome Evaluation System characterizes the effectiveness of consultative activities. The initial phase of the system identifies consultees' responses to psychiatric consultants' recommendations and diagnoses and the variables critical to concordance with the use of quantitative measures. The observed incidence and concordance rates of the consultant-consultee interaction were integrated (1) to establish a concordance hierarchy clarifying consultees' priorities in seeking psychiatric consultation, (2) to provide reference points to guide psychiatric consultants' clinical actions, (3) to establish tentative standards with which to evaluate the effectiveness of psychiatric consultation, and (4) to signal the need for further outcome studies and the development of data-based consultation practices.

Clinical Competence↗

PubMed1977

A brush-border-bound peptidase and amino acid transport.

Aminopeptidase when in its integral form interacts with lecithin to form a stable lipoprotein complex. The reconstituted system is a single-bilayer vesicle about 30 nm in diameter. The hydrophobic part of the amphipathic hydrolase is incorporated in the lecithin bilayer with the portion carrying enzymic activity oriented towards the external aqueous phase. This part can be detached by proteases.

Amino Acids↗

PubMed1979

Loss of thick filaments from fast-twitch glucolytic muscle fibers of the pigeon pectoralis after chronic administration of dantrolene sodium.

Adult pigeons received dantrolene sodium, a skeletal muscle relaxant which blocks the release of calcium during excitation-contraction coupling, for 12 to 16 weeks. The pectoralis muscles of these birds were analyzed for changes occurring in the various fiber types of the muscle. Both histochemistry (ATPase and SDH activity) and electron microscopy (mitochondrial and lipid volume percentages) differentiated two fiber types. The two fiber-types consisted of fast-twitch glycolytic fibers (FG) and fast-twitch oxidative-glycolytic (FOG) fibers. After dantrolene treatment some FG fibers showed little or no ATPase activity. Dantrolene treatment also produced a disappearance of thick filaments in some FG fibers. We infer that the fibers without thick filaments are the ones lacking ATPase activity. The FOG fibers were nearly normal. Since drug-fed birds lose weight, a few birds were starved to determine whether the filament loss was related solely to the bird's loss in weight. No fibers in starved birds showed reduced ATPase activity or loss of thick filaments. In fibers that showed thick filament disappearance, the I-bands remained organized and intact, suggesting that the I-band maintains its integrity without interaction with the thick filaments. Changes in activity patterns may cause loss of thick filaments by inhibiting either their synthesis or assembly.

Adenosine Triphosphatases↗

PubMed2026

Transcriptomic Profiling Reveals NF-κB-Associated Immune Regulatory Signatures Underlying the Regenerative Effects of Hypoxia-Preconditioned Tendon Stem Cell-Derived Extracellular Vesicles.

Remodeling of the immune microenvironment is a critical determinant of tissue regeneration, yet the molecular programs associated with the enhanced therapeutic activity of hypoxia-preconditioned extracellular vesicles remain incompletely defined. In this study, we investigated the regenerative and immunomodulatory effects of hypoxia-preconditioned tendon stem cell-derived extracellular vesicles (Hypo-EVs) and employed transcriptomic profiling to identify molecular signatures associated with their biological activity. The therapeutic effects of Hypo-EVs were evaluated using a rat patellar tendon defect model and lipopolysaccharide-stimulated RAW 264.7 macrophages. Histological analysis, immunostaining, biomechanical testing, and reverse transcription-quantitative polymerase chain reaction were performed to assess tendon healing and macrophage polarization, while RNA sequencing was conducted in macrophages treated with Hypo-EVs or normoxia-derived EVs, followed by Gene Set Enrichment Analysis, Gene Ontology, and Kyoto Encyclopaedia of Genes and Genomes pathway analyses. Hypo-EVs significantly alleviated local inflammatory responses, improved collagen organization and biomechanical properties of repaired tendons, and promoted macrophage polarization toward a reparative M2 phenotype both in vivo and in vitro. Consistent with these biological effects, transcriptomic profiling revealed extensive remodeling of inflammation-related gene expression programs, including significant suppression of NF-κB, TNF, IL-17, and cytokine-cytokine receptor interaction pathways. Integrative bioinformatic analyses identified an NF-κB-associated immune-regulatory signature that distinguished Hypo-EV-treated macrophages from those receiving normoxic EVs. Mechanistically, Hypo-EVs attenuated NF-κB activation, as evidenced by reduced phosphorylation of p65 and IκBα, whereas TNF-α-mediated NF-κB activation partially diminished their macrophage-repolarizing effects. Collectively, these findings demonstrate that hypoxic preconditioning enhances the immunomodulatory and regenerative functions of tendon stem cell-derived EVs. Transcriptomic analyses identified an NF-κB-associated immune-regulatory signature linked to the biological activity of Hypo-EVs, providing a molecular framework for understanding EV-mediated immune modulation and supporting the development of transcriptome-guided molecular signatures for regenerative therapies targeting tendon immune homeostasis.

Animals↗

PubMed2003

Spatiotemporal gradient of oligodendrocyte differentiation in chick optic tectum requires brain integrity and cell-cell interactions.

The development of oligodendrocytes in the chicken optic tectum (OT) was studied in vivo and in vitro by analyzing expression of myelin-associated glycoprotein (MAG) with a monoclonal antibody. MAG(+) cells first appeared in the anterior OT on embryonic day (E) 12, were present throughout the anterior half on E15, and eventually filled the tectum on E17. This spatiotemporal appearance of MAG(+) oligodendrocytes resembled two streams of cells entering the OT along the afferent and efferent axonal layers. However, experiments determined that this appearance of MAG immunoreactivity was the result of a gradient of oligodendrocyte differentiation and was not cell migration. First, retroviral vector labeling of OT progenitors in vivo on E3 resulted in labeled oligodendrocytes in late embryos. In addition, pieces of OT from as early as E3 kept in culture for a week developed numerous MAG(+) oligodendrocytes. Pieces of both anterior and posterior E7 OT developed MAG(+) oligodendrocytes after 3 days in culture, well ahead of their normal schedule in vivo. BrdU incorporation studies revealed that these cells were not born in culture, but merely differentiated. Monolayer cultures made from dissociated E10 or later OT cells developed MAG(+) oligodendrocytes, but monolayers made from E7 OT cells did not. These experiments demonstrate that oligodendrocyte progenitors were present in the OT as early as E3, that they could differentiate precociously, and that their normal progressive differentiation in situ must be due to removal of inhibitory constraints rather than the onset of inductive factors. Also, certain cell-cell interactions occur between E7 and E10, which cannot be disrupted if oligodendrocyte differentiation is to occur.

Animals↗

PubMed1995

Chemotaxis and phototaxis require a CheA histidine kinase in the archaeon Halobacterium salinarium.

Histidine kinases are part of the two-component signal transduction system responsible for eubacterial responses to diverse environmental signals. They have recently been detected in eukaryotes but their existence in the kingdom Archaea remains uncertain. Here we report the sequence and function of a histidine kinase (CheAH.s.) from Halobacterium salinarium, the first such transmitter in Archaea. The protein CheAH.s. (668 residues) has significant sequence identity with the CheA proteins known from eubacterial signal transduction (e.g. 34% identity with CheA from Bacillus subtilis). Antibodies were raised against CheAH.s. as expressed in Escherichia coli and were used in Western blotting to demonstrate the expression of cheAH.s. in H. salinarium. As has been observed for other halophilic proteins, CheAH.s. has a deviant electrophoretic migration, with an apparent molecular weight of 103 kDa on SDS-PAGE compared with a calculated molecular weight of 72 kDa. Deletion of a part of the cheAH.s. gene leads to loss of both chemotactic and phototactic responses in H. salinarium as measured by swarm plate assays, motion analysis and tethering experiments. This indicates that CheAH.s. plays a crucial role in chemical and light signal integration, presumably interacting with at least two phototransducers and a number of chemoreceptors.

Amino Acid Sequence↗