scholarly journals Interplay between OmpA and RpoN Regulates Flagellar Synthesis in Stenotrophomonas maltophilia

2021 ◽  
Vol 9 (6) ◽  
pp. 1216
Author(s):  
Chun-Hsing Liao ◽  
Chia-Lun Chang ◽  
Hsin-Hui Huang ◽  
Yi-Tsung Lin ◽  
Li-Hua Li ◽  
...  
Keyword(s):  
Stenotrophomonas Maltophilia ◽  
Protein A ◽  
Underlying Mechanism ◽  
Hierarchical Organization ◽  
Qrt Pcr ◽  
Regulatory Cascade ◽  
Promising Target ◽  
And Function ◽  
The Relationship ◽  
Abundant Transcript

OmpA, which encodes outer membrane protein A (OmpA), is the most abundant transcript in Stenotrophomonas maltophilia based on transcriptome analyses. The functions of OmpA, including adhesion, biofilm formation, drug resistance, and immune response targets, have been reported in some microorganisms, but few functions are known in S. maltophilia. This study aimed to elucidate the relationship between OmpA and swimming motility in S. maltophilia. KJΔOmpA, an ompA mutant, displayed compromised swimming and failure of conjugation-mediated plasmid transportation. The hierarchical organization of flagella synthesis genes in S. maltophilia was established by referencing the Pseudomonas aeruginosa model and was confirmed using mutant construction, qRT-PCR, and functional assays. Distinct from the P. aeruginosa model, rpoN, rather than fleQ and fliA, was at the top of the flagellar regulatory cascade in S. maltophilia. To elucidate the underlying mechanism responsible for ΔompA-mediated swimming compromise, transcriptome analysis of KJ and KJΔOmpA was performed and revealed rpoN downregulation in KJΔOmpA as the key element. The involvement of rpoN in ΔompA-mediated swimming compromise was verified using rpoN complementation, qRT-PCR, and function assays. Collectively, OmpA, which contributes to bacterial conjugation and swimming, is a promising target for adjuvant design in S. maltophilia.

HIERARCHICAL ORGANIZATION AND DISASSORTATIVE MIXING OF CORRELATION-BASED WEIGHTED FINANCIAL NETWORKS

2010 ◽  
Vol 21 (03) ◽  
pp. 433-441 ◽  
Author(s):  
SHI-MIN CAI ◽  
YAN-BO ZHOU ◽  
TAO ZHOU ◽  
PEI-LING ZHOU
Keyword(s):  
Financial Market ◽  
Span Tree ◽  
Nearest Neighbor ◽  
Underlying Mechanism ◽  
Hierarchical Organization ◽  
Cumulative Distribution ◽  
Financial Networks ◽  
Financial Network ◽  
Weighted Complex Network ◽  
The Relationship

Correlation-based weighted financial networks are analyzed to present cumulative distribution of strength with a power-law tail, which suggests that a small number of hub-like stocks have greater influence on the whole fluctuation of financial market than others. The relationship between clustering and connectivity of vertices emphasizes hierarchical organization, which has been depicted by minimal span tree in previous work. These results urge us to further study the mixing patter of financial network to understand the tendency for vertices to be connected to vertices that are like (or unlike) them in some way. The measurement of average nearest-neighbor degree running over classes of vertices with degree k shows a descending trend when k increases. This interesting result is first uncovered in our work, and suggests the disassortative mixing of financial network which refers to a bias in favor of connections between dissimilar vertices. All the results in weighted complex network aspect may provide some insights to deeper understand the underlying mechanism of financial market and model the evolution of financial market.

scholarly journals Distinct Expression and Function of Alternatively Spliced Tbx5 Isoforms in Cell Growth and Differentiation

2008 ◽  
Vol 28 (12) ◽  
pp. 4052-4067 ◽  
Author(s):  
Romain Georges ◽  
Georges Nemer ◽  
Martin Morin ◽  
Chantal Lefebvre ◽  
Mona Nemer
Keyword(s):  
Heart Development ◽  
Wide Spectrum ◽  
Protein A ◽  
Growth Stimulation ◽  
Underlying Mechanism ◽  
Experimental Models ◽  
Dependent Manner ◽  
Dominant Disease ◽  
And Function

ABSTRACT Mutations in the T-box transcription factor Tbx5 cause Holt-Oram syndrome, an autosomal dominant disease characterized by a wide spectrum of cardiac and upper limb defects with variable expressivity. Tbx5 haploinsufficiency has been suggested to be the underlying mechanism, and experimental models are consistent with a dosage-sensitive requirement for Tbx5 in heart development. Here, we report that Tbx5 levels are regulated through alternative splicing that generates, in addition to the known 518-amino-acid protein, a C-terminal truncated isoform. This shorter isoform retains the capacity to bind DNA, but its interaction with Tbx5 collaborators such as GATA-4 is altered. In vivo, the two spliced isoforms are oppositely regulated in a temporal and growth factor-dependent manner and are present in distinct DNA-binding complexes. The expression of the long isoform correlates with growth stimulation, and its reexpression in postnatal transgenic mouse hearts promotes hypertrophy. Conversely, the upregulation of the short but not the long isoform in C2C12 myoblasts leads to growth arrest and cell death. The results provide novel insight into posttranscriptional Tbx5 regulation and point to an important role not only in cell differentiation but also in cell proliferation and organ growth. The data may help analyze genotype-phenotype relations in patients with Holt-Oram syndrome.

scholarly journals Personalized medicine in cystic fibrosis: genistein supplementation as a treatment option for patients with a rare S1045Y-CFTR mutation

2016 ◽  
Vol 311 (2) ◽  
pp. L364-L374 ◽  
Author(s):  
Kavisha Arora ◽  
Sunitha Yarlagadda ◽  
Weiqiang Zhang ◽  
ChangSuk Moon ◽  
Erin Bouquet ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Tyrosine Phosphorylation ◽  
Stop Codon ◽  
Protein A ◽  
Underlying Mechanism ◽  
Surface Expression ◽  
African American Patient ◽  
American Patient ◽  
Cf Transmembrane Conductance Regulator ◽  
And Function

Cystic fibrosis (CF) is a life-shortening disease caused by the mutations that generate nonfunctional CF transmembrane conductance regulator (CFTR) protein. A rare serine-to-tyrosine (S1045Y) CFTR mutation was earlier reported to result in CF-associated fatality. We identified an African-American patient with the S1045Y mutation in CFTR, as well as a stop-codon mutation, who has a mild CF phenotype. The underlying mechanism of CF caused by S1045Y-CFTR has not been elucidated. In this study, we determined that S1045Y-CFTR exhibits twofold attenuated function compared with wild-type (WT)-CFTR. We report that serine-to-tyrosine mutation leads to increased tyrosine phosphorylation of S1045Y-CFTR, followed by recruitment and binding of E3-ubiquitin ligase c-cbl, resulting in enhanced ubiquitination and passage of S1045Y-CFTR in the endosome/lysosome degradative compartments. We demonstrate that inhibition of tyrosine phosphorylation partially rescues S1045Y-CFTR surface expression and function. Based on our findings, it could be suggested that consuming genistein (a tyrosine phosphorylation inhibitor) would likely ameliorate CF symptoms in individuals with S1045Y-CFTR, providing a unique personalized therapy for this rare CF mutation.

scholarly journals Circle RNA PLEC Acts as a Sponge of Microrna-198 to Promote Gastric Carcinoma Cell Resistance to Paclitaxel and Tumorigenesis

2021 ◽  
Author(s):  
Ning Zhou ◽  
Wei Wang ◽  
Chunlei Xu ◽  
Wenyan Yu
Keyword(s):  
Bioinformatics Analysis ◽  
Carcinoma Cell ◽  
Underlying Mechanism ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cell Resistance ◽  
Qrt Pcr ◽  
Reporter Assays ◽  
Fcm Analysis ◽  
The Relationship

Abstract Gastric carcinoma (GC) is one of the most frequent type of malignancy all over the world. The resistance of Paclitaxel (PTX) has become the obstacle of the prognosis of GC, and the underlying mechanism of is not clear. Previous study showed that GC-related circRNAs have been identified via microarray analysis and bioinformatics analysis, and we discovered that circPLEC (hsa_circ_0085923) remarkably upregulated in GC cells. The molecular mechanism of circPLEC in PTX-resistance GC cells still needs to explore.The expression of circPLEC in GC cells, PTX-resistant GC cells and GC tissues was analyzed by qRT-PCR. CircPLEC was knocked down in GC cells by transfecting shRNA, and then we used the CCK-8 assay, transwell, and FCM analysis to verify the effect in circPLEC in PTX-resistant GC cells. Additionally, we used luciferase reporter assays to confirm the relationship among circPLEC, miR-198 and MUC19.In present study, qRT-PCR exhibited that circPLEC were upregulated in PTX-resistant GC tissues and cells, indicating that circPLEC boost the PTX resistance of GC. circPLEC downregulation could weaken the GC resistance to PTX and the ability of tumorigenesis, migration and invasion, and promote the apoptosis of PTX-resistant GC cells. miR-198 inhibitor could revise the effect of circPLEC downregulation in PTX-resistant GC cells, and MUC19 downregulation could weaken the GC resistance to PTX and the tumorigenesis, and improve the apoptosis of PTX-resistant GC cells. In summary, circPLEC acts as a sponge of miR-198 to promote the PTX resistance and tumorigenesis of GC cells by regulating MUC19 expression.

scholarly journals Regulation of the integrin αVβ3- actin filaments axis in early osteogenesis of human fibroblasts under cyclic tensile stress

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yan Peng ◽  
Rongmei Qu ◽  
Yanting Feng ◽  
Xiaolan Huang ◽  
Yuchao Yang ◽  
...  
Keyword(s):  
Tensile Stress ◽  
Osteogenic Differentiation ◽  
Human Fibroblasts ◽  
Integrin Αvβ3 ◽  
Cytochalasin D ◽  
Qrt Pcr ◽  
Lentivirus Transduction ◽  
And Function ◽  
The Relationship ◽  
Positive Effect

Abstract Background Integrins play a prominent role in osteogenic differentiation by transmitting both mechanical and chemical signals. Integrin expression is closely associated with tensile stress, which has a positive effect on osteogenic differentiation. We investigated the relationship between integrin αVβ3 and tensile stress. Methods Human fibroblasts were treated with c (RGDyk) and lentivirus transduction to inhibit function of integrin αVβ3. Y-15, cytochalasin D and verteporfin were used to inhibit phosphorylation of FAK, polymerization of microfilament and function of nuclear YAP, respectively. Fibroblasts were exposed to a cyclic tensile stress of 10% at 0.5 Hz, once a day for 2 h each application. Fibroblasts were harvested on day 4 and 7 post-treatment. The expression of ALP, RUNX2, integrin αVβ3, β-actin, talin-1, FAK, vinculin, and nuclear YAP was detected by Western blot or qRT-PCR. The expression and distribution of integrin αVβ3, vinculin, microfilament and nuclear YAP. Results Cyclic tensile stress was found to promote expression of ALP and RUNX2. Inhibition of integrin αVβ3 activation downregulated the rearrangement of microfilament and the expression of ALP, RUNX2 and nuclear YAP. When the polymerization of microfilament was inhibited the expression of ALP, RUNX2 and nuclear YAP were decreased. The phosphorylation of FAK induced by cyclic tensile stress reduced by the inhibition of integrin αVβ3. The expression of ALP and RUNX2 was decreased by inhibition of phosphorylation of FAK and inhibition of nuclear YAP. Conclusions Cyclic tensile stress promotes osteogenesis of human fibroblasts via integrin αVβ3-microfilament axis. Phosphorylation of FAK and nuclear YAP participates in this process.

scholarly journals Active establishment of centromeric CENP-A chromatin by RSF complex

2009 ◽  
Vol 185 (3) ◽  
pp. 397-407 ◽  
Author(s):  
Marinela Perpelescu ◽  
Naohito Nozaki ◽  
Chikashi Obuse ◽  
Hua Yang ◽  
Kinya Yoda
Keyword(s):  
Protein A ◽  
Centromeric Chromatin ◽  
Daughter Cells ◽  
Centromere Protein ◽  
Centromere Protein A ◽  
Protein Components ◽  
And Function ◽  
Relationship Of ◽  
The Relationship

Centromeres are chromosomal structures required for equal DNA segregation to daughter cells, comprising specialized nucleosomes containing centromere protein A (CENP-A) histone, which provide the basis for centromeric chromatin assembly. Discovery of centromere protein components is progressing, but knowledge related to their establishment and maintenance remains limited. Previously, using anti-CENP-A native chromatin immunoprecipitation, we isolated the interphase–centromere complex (ICEN). Among ICEN components, subunits of the remodeling and spacing factor (RSF) complex, Rsf-1 and SNF2h proteins, were found. This paper describes the relationship of the RSF complex to centromere structure and function, demonstrating its requirement for maintenance of CENP-A at the centromeric core chromatin in HeLa cells. The RSF complex interacted with CENP-A chromatin in mid-G1. Rsf-1 depletion induced loss of centromeric CENP-A, and purified RSF complex reconstituted and spaced CENP-A nucleosomes in vitro. From these data, we propose the RSF complex as a new factor actively supporting the assembly of CENP-A chromatin.

The relationship of IGE receptor topography to signaling activity in RBL-2H3 mast cells

1991 ◽  
Vol 49 ◽  
pp. 236-237
Author(s):  
J.R. Pfeiffer ◽  
J.C. Seagrave ◽  
C. Wofsy ◽  
J.M. Oliver
Keyword(s):  
Mast Cells ◽  
Protein A ◽  
Scattered Electron ◽  
Ige Receptor ◽  
Receptor Complexes ◽  
Ige Binding ◽  
Electron Imaging ◽  
Small Clusters ◽  
Relationship Of ◽  
The Relationship

In RBL-2H3 rat leukemic mast cells, crosslinking IgE-receptor complexes with anti-IgE antibody leads to degranulation. Receptor crosslinking also stimulates the redistribution of receptors on the cell surface, a process that can be observed by labeling the anti-IgE with 15 nm protein A-gold particles as described in Stump et al. (1989), followed by back-scattered electron imaging (BEI) in the scanning electron microscope. We report that anti-IgE binding stimulates the redistribution of IgE-receptor complexes at 37“C from a dispersed topography (singlets and doublets; S/D) to distributions dominated sequentially by short chains, small clusters and large aggregates of crosslinked receptors. These patterns can be observed (Figure 1), quantified (Figure 2) and analyzed statistically. Cells incubated with 1 μg/ml anti-IgE, a concentration that stimulates maximum net secretion, redistribute receptors as far as chains and small clusters during a 15 min incubation period. At 3 and 10 μg/ml anti-IgE, net secretion is reduced and the majority of receptors redistribute rapidly into clusters and large aggregates.

Scanning tunneling microscopy (STM) of DNA and RNA

1989 ◽  
Vol 47 ◽  
pp. 34-35
Author(s):  
Patricia G. Arscott ◽  
Gil Lee ◽  
Victor A. Bloomfield ◽  
D. Fennell Evans
Keyword(s):  
Molecular Structures ◽  
Inorganic Materials ◽  
Resolving Power ◽  
Scanning Tunneling ◽  
Tunneling Microscopy ◽  
Form And Function ◽  
Dna And Rna ◽  
Calf Thymus ◽  
And Function ◽  
The Relationship

STM is one of the most promising techniques available for visualizing the fine details of biomolecular structure. It has been used to map the surface topography of inorganic materials in atomic dimensions, and thus has the resolving power not only to determine the conformation of small molecules but to distinguish site-specific features within a molecule. That level of detail is of critical importance in understanding the relationship between form and function in biological systems. The size, shape, and accessibility of molecular structures can be determined much more accurately by STM than by electron microscopy since no staining, shadowing or labeling with heavy metals is required, and there is no exposure to damaging radiation by electrons. Crystallography and most other physical techniques do not give information about individual molecules.We have obtained striking images of DNA and RNA, using calf thymus DNA and two synthetic polynucleotides, poly(dG-me5dC)·poly(dG-me5dC) and poly(rA)·poly(rU).

Structure and Function of Angiopoietin-like Protein 3 (ANGPTL3) in Atherosclerosis

2020 ◽  
Vol 27 (31) ◽  
pp. 5159-5174 ◽  
Author(s):  
Xinjie Lu
Keyword(s):  
Low Density Lipoprotein ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Structure And Function ◽  
Biological Functions ◽  
Pharmacological Management ◽  
Vascular Growth ◽  
Promising Target ◽  
And Function ◽  
Systematic Appraisal

Background:Angiopoietin-Like Proteins (ANGPTLs) are structurally related to the angiopoietins. A total of eight ANGPTLs (from ANGPTL1 to ANGPTL8) have been identified so far. Most ANGPTLs possess multibiological functions on lipid metabolism, atherosclerosis, and cancer. Among them, ANGPTL3 has been shown to regulate the levels of Very Low-Density Lipoprotein (VLDL) made by the liver and play a crucial role in human lipoprotein metabolism.Method:A systematic appraisal of ANGPTLs was conducted, focusing on the main features of ANGPTL3 that has a significant role in atherosclerosis.Results:Angiopoietins including ANGPTL3 are vascular growth factors that are highly specific for endothelial cells, perform a variety of other regulatory activities to influence inflammation, and have been shown to possess both pro-atherosclerotic and atheroprotective effects.Conclusion:ANGPTL3 has been demonstrated as a promising target in the pharmacological management of atherosclerosis. However, many questions remain about its biological functions.

MiR-493 Induces Cytotoxic Autophagy in Prostate Cancer Cells through Regulation on PHLPP2

2020 ◽  
Vol 21 (14) ◽  
pp. 1451-1456 ◽  
Author(s):  
Jun Deng ◽  
Ming Ma ◽  
Wei Jiang ◽  
Liangliang Zheng ◽  
Suping Cui
Keyword(s):  
Prostate Cancer ◽  
Protein Expression ◽  
Cell Function ◽  
Mrna Levels ◽  
Prostate Cancer Cells ◽  
Potent Inducer ◽  
Qrt Pcr ◽  
Autophagy Gene ◽  
The Relationship ◽  
Cancer Inhibition

Background: MiR-493 promotes the proliferation of prostate cancer (PC) cells by targeting PHLPP2. We aimed to explore the relationship between miR-493 and autophagy in PC. Methods: qRT-PCR and western blotting were used to determine the mRNA levels and protein expression of miR-493, PHLPP2, autophagy gene BECN1 and ATG7 in PC cells. The autophagy gene expression was determined after PC cells transfected with miR-493 precursor or PHLPP2 precursor. Corresponding changes of autophagy phenotype and PC cell function were also studied. Results: The mRNA levels and protein expression of miR-493, PHLPP2, BECN1 and ATG7 in PC cells were significantly decreased in PC cells. Overexpression of miR-493 or PHLPP2 markedly upregulated the expression levels of BECN1 and ATG7 in PC cells. Overexpression of miR-493 and PHLPP2 markedly promoted autophagy, and inhibited the invasion and cloning formation of PC cells. Conclusion: MiR-493 is a potent inducer of cytotoxic autophagy that leads to prostate cancer inhibition by regulating on PHLPP2.

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