scholarly journals The oncornavirus glycoprotein gp69/71: a constituent of the surface of normal and malignant thymocytes.

1975 ◽  
Vol 141 (1) ◽  
pp. 172-187 ◽  
Author(s):  
B C Del Vellano ◽  
B Nave ◽  
B P Croker ◽  
R A Lerner ◽  
F J Dixon
Keyword(s):  
Leukemia Virus ◽  
Molecular Size ◽  
Size Class ◽  
Antigenic Determinants ◽  
Lymphoma Cells ◽  
Differentiated Cells ◽  
Interesting Difference ◽  
Associated Proteins ◽  
Related Proteins ◽  
The Relationship

The oncornavirus related proteins associated with the surface of normal and malignant thymocytes were studied. Three virion-associated proteins (gp69/71, p45, p30) were associated with lymphoma cells from about 70% of the tumors studied. Two virion-associated proteins (gp69/71 and p45 were associated with normal thymocytes form some but not all strains of mice. In gp69/71- mice, conversion to the gp69/71+ phenotype accompanied leukemogenesis. An interesting difference in the apparent molecular size of virus related antigens of the 70,000 dalton size class was detected in lymphoma cells present in involved spleens as compared to involved thymuses. Mice infected as neonates with Scripps leukemia virus make antibody to gp69/71 and some make antibodies to molecules associated with the surface of their own tumors. The significance of the restricted presence of antigens coded for by the viral genome to the surface of some differentiated cells is discussed in reference to (a) the relationship between virion, leukemia associated, and differentiation dependent markers, and (b) the possible consequence to the host of having similar antigenic determinants on three independent structures with replicative potential (virus, normal thymocytes, and tumor cells).

Alzheimer's Paired Helical Filaments Contain Insoluble Cytoskeletal Elements

1985 ◽  
Vol 43 ◽  
pp. 748-751
Author(s):  
P. Gambetti ◽  
G. Perry ◽  
L. Autillo-Gambetti
Keyword(s):  
Paired Helical Filaments ◽  
Microscope Level ◽  
Antigenic Determinants ◽  
Light Microscope Level ◽  
Neuronal Cytoskeleton ◽  
Ionic Detergent ◽  
Associated Proteins ◽  
Pathologic Lesions ◽  
10 Nm Filaments ◽  
Cytoskeletal Elements

Neurofibrillary tangles (NFT) are one of the major pathologic lesions of Alzheimer's disease. These neuronal inclusions are predominantly composed of paired helical filaments (PHF), which consist of two 10 nm filaments winding around each other with an approximately 80 nm periodicity. Besides PHF, NFT comprise also 15 nm filaments, 10 nm filaments which are probably neurofilaments, microtubules and granular material. At variance with the neuronal cytoskeleton, PHF are insoluble in ionic detergent.Studies at the light microscope level have shown that NFT have unique antigenic determinants as well as determinants in common with elements of the normal neuronal cytoskeleton such as neurofilaments and microtubule-associated proteins. The present study uses immunocytochemistry and cytochemistry at the electron microscope level to assess which NFT component contains these determinants and whether these antigenic determinants are soluble in an ionic detergent.

scholarly journals The relationship of indoxyl sulfate and p-cresyl sulfate with target cardiovascular proteins in hemodialysis patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ping-Hsun Wu ◽  
Yi-Ting Lin ◽  
Yi-Wen Chiu ◽  
Gabriel Baldanzi ◽  
Jiun-Chi Huang ◽  
...  
Keyword(s):  
Hemodialysis Patients ◽  
Complement Component ◽  
Uremic Toxins ◽  
Indoxyl Sulfate ◽  
Free Form ◽  
Negatively Associated ◽  
Coronary Syndrome ◽  
Increased Risk ◽  
Related Proteins ◽  
The Relationship

AbstractProtein-bound uremic toxins (Indoxyl sulfate [IS] and p-cresyl sulfate [PCS]) are both associated with cardiovascular (CV) and all-cause mortality in subjects with chronic kidney disease (CKD). Possible mechanisms have not been elucidated. In hemodialysis patients, we investigated the relationship between the free form of IS and PCS and 181 CV-related proteins. First, IS or PCS concentrations were checked, and high levels were associated with an increased risk of acute coronary syndrome (ACS) in 333 stable HD patients. CV proteins were further quantified by a proximity extension assay. We examined associations between the free form protein-bound uremic toxins and the quantified proteins with correction for multiple testing in the discovery process. In the second step, the independent association was evaluated by multivariable-adjusted models. We rank the CV proteins related to protein-bound uremic toxins by bootstrapped confidence intervals and ascending p-value. Six proteins (signaling lymphocytic activation molecule family member 5, complement component C1q receptor, C–C motif chemokine 15 [CCL15], bleomycin hydrolase, perlecan, and cluster of differentiation 166 antigen) were negatively associated with IS. Fibroblast growth factor 23 [FGF23] was the only CV protein positively associated with IS. Three proteins (complement component C1q receptor, CCL15, and interleukin-1 receptor-like 2) were negatively associated with PCS. Similar findings were obtained after adjusting for classical CV risk factors. However, only higher levels of FGF23 was related to increased risk of ACS. In conclusion, IS and PCS were associated with several CV-related proteins involved in endothelial barrier function, complement system, cell adhesion, phosphate homeostasis, and inflammation. Multiplex proteomics seems to be a promising way to discover novel pathophysiology of the uremic toxin.

scholarly journals Scanning Electron-Assisted Dielectric Microscopy Reveals Autophagosome Formation by LC3 and ATG12 in Cultured Mammalian Cells

2021 ◽  
Vol 22 (4) ◽  
pp. 1834
Author(s):  
Tomoko Okada ◽  
Toshihiko Ogura
Keyword(s):  
Mammalian Cells ◽  
Culture Medium ◽  
Related Gene ◽  
Autophagosome Formation ◽  
Intact Cells ◽  
Microtubule Associated Proteins ◽  
Associated Proteins ◽  
The Difference ◽  
Related Proteins ◽  
Scanning Electron

Autophagy is an intracellular self-devouring system that plays a central role in cellular recycling. The formation of functional autophagosomes depends on several autophagy-related proteins, including the microtubule-associated proteins 1A/1B light chain 3 (LC3) and the conserved autophagy-related gene 12 (Atg12). We have recently developed a novel scanning electron-assisted dielectric microscope (SE-ADM) for nanoscale observations of intact cells. Here, we used the SE-ADM system to observe LC3- and Atg12-containing autophagosomes in cells labelled in the culture medium with antibodies conjugated to colloidal gold particles. We observed that, during autophagosome formation, Atg12 localized along the actin meshwork structure, whereas LC3 formed arcuate or circular alignments. Our system also showed a difference in the distribution of LC3 and Atg12; Atg12 was broadly distributed while LC3 was more localized. The difference in the spatial distribution demonstrated by our system explains the difference in the size of fluorescent spots due to the fluorescently labelled antibodies observed using optical microscopy. The direct SE-ADM observation of cells should thus be effective in analyses of autophagosome formation.

MicroRNA-487a-3p Regulates the Senescence of Mesenchymal Stem Cells by Targeting Silencing Information Regulator-Associated Enzyme 1 (SIRT1)

2021 ◽  
Vol 11 (8) ◽  
pp. 1576-1581
Author(s):  
Yiwei Shen ◽  
Xue Li ◽  
Xiaoke Wu ◽  
Yi Li ◽  
Yiwei Shen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cellular Senescence ◽  
Control Group ◽  
Human Mscs ◽  
Galactosidase Activity ◽  
Activity Staining ◽  
Plasmid Transfection ◽  
Related Proteins ◽  
The Relationship

SIRT1 is known to be closely associated with cellular senescence, while the relationship between miR-487a-3p and SIRT1 and their role in mesenchymal stem cells (MSCs) remains unclear. MiRDB analysis showed SIRT1 is a target of miR-487a-3p. Here we investigated whether miR-487a-3p modulates senescence of mesenchymal stem cells by targeting SIRT1. The human MSCs (hMSCs) were divided into control group (NC group), miR-487a-3p Mimics group, pCMV-SIRT+miR-487a-3p Mimics group followed by analysis of miR-487a-3p expression by qPCR and protein level of SIRT1, P21 and P53 by western blot. Dual luciferin report assay verified the binding of miR-487a-3p to SIRT1 mRNA and β-galactosidase activity staining detected hMSCs senescence. miR-487a-3p level was significantly elevated after miR-487a-3p Mimics treatment (P <0.01) without difference between miR-487a-3p Mimics group and pCMV-SIRT1 group+miR-487a-3pMimics (P >0.05). miR-487a-3p mimics significantly decreased SIRT1 level (P < 0.01), which was reversed by pCMVSIRT1 plasmid transfection (P <0.05). Moreover, miR-487a-3p could bind SIRT1 mRNA 3′-UTR region. Further more, miR-487a-3p Mimics induced cellular senescence as displayed by increased β-galactosidase activity (P <0.01) and increased level of senescence-related proteins P21 and P53 (P < 0.01), which were all reversed by overexpression of SIRT1 (P < 0.05). In conclusion, miR-487a-3p reduced SIRT1 expression, thus promoting hMSCs senescence, while overexpression of SIRT1 could counteract the senescence of hMSCs induced by miR-487a-3p.

scholarly journals Retroviral Restriction Factors Fv1 and TRIM5α Act Independently and Can Compete for Incoming Virus before Reverse Transcription

2006 ◽  
Vol 80 (5) ◽  
pp. 2100-2105 ◽  
Author(s):  
Luca D. Passerini ◽  
Zuzana Keckesova ◽  
Greg J. Towers
Keyword(s):  
Life Cycle ◽  
Reverse Transcription ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Viral Life Cycle ◽  
Human Cells ◽  
Restriction Factors ◽  
Retroviral Infection ◽  
The Relationship ◽  
Murine Leukemia

ABSTRACT The restriction factors Fv1 and TRIM5α provide dominant blocks to retroviral infection, targeting incoming capsids at a postentry, preintegration step. They both restrict N-tropic murine leukemia virus with similar specificity yet act at different points in the viral life cycle. TRIM5α-restricted virus is usually unable to reverse transcribe, whereas Fv1-restricted virus reverse transcribes normally. Here we investigate the relationship between these two restriction factors by expressing Fv1 alleles in human cells. We demonstrate that Fv1 is able to compete with TRIM5α for virus before reverse transcription. In human cells expressing Fv1b, N-tropic restricted virus becomes less infectious but reverse transcribes more efficiently, indicating competition between the two antiviral molecules and protection of the virus from TRIM5α by Fv1. Our findings suggest that, like TRIM5α, Fv1 interacts with virus before reverse transcription, but the consequences of this interaction are not realized until a later stage of the life cycle. We also demonstrate that Fv1 is functionally independent of TRIM5α when expressed in human cells.

scholarly journals Expression of the third member of the serum amyloid A gene family in mouse adipocytes.

1989 ◽  
Vol 169 (5) ◽  
pp. 1841-1846 ◽  
Author(s):  
E P Benditt ◽  
R L Meek
Keyword(s):  
Serum Amyloid A ◽  
Cell System ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Differentiated Cells ◽  
Homologous Genes ◽  
Extrahepatic Tissues ◽  
Mouse Adipocytes ◽  
Related Proteins

Three homologous genes that code for three related proteins comprise the serum amyloid A (SAA) family in the mouse. Endotoxin induces equally vigorous expression of mRNAs for the three SAA genes in liver. In extrahepatic tissues SAA1 and/or SAA2 mRNAs have been found only in kidney and intestine, however, SAA3 is expressed in all extrahepatic tissues thus far examined. This observation raised the question: is SAA3 mRNA expressed by a single cell system dispersed throughout all tissues, or by differentiated cells of each tissue? This question was explored in various tissues by in situ hybridization with a single-stranded cRNA probe specific for SAA3 mRNA. We found expression in the liver of SAA3 mRNA by other cells as well as by hepatocytes. A common feature among extrahepatic tissues was SAA3 mRNA expression in adipocytes. SAA3 mRNA was also found in two nonadipose cells, Leydig cells of the testis, and some of the cells located in parafollicular zones of the spleen.

scholarly journals Plant Phenolics as Pathogen-Carrier Immunogenicity Modulator Haptens

2020 ◽  
Vol 21 (10) ◽  
pp. 897-905
Author(s):  
Castillo-Maldonado Irais ◽  
Sevilla-González María-de-la-Luz ◽  
Delgadillo-Guzmán Dealmy ◽  
Ramírez-Moreno Agustina ◽  
Cabral-Hipólito Nidia ◽  
...  
Keyword(s):  
Phenolic Compounds ◽  
Protein Interactions ◽  
Structural Complexity ◽  
Molecular Size ◽  
Structural Heterogeneity ◽  
Antigenic Determinants ◽  
Plant Phenolics ◽  
Protein Protein Interactions ◽  
Related Factors ◽  
Molecular Events

Background: Pathogens use multiple mechanisms to disrupt cell functioning in their host and allow pathogenesis. These mechanisms involve communication between the pathogen and the host cell through protein-protein interactions. Methods: Protein-protein interactions chains referred to as signal transduction pathways are the processes by which a chemical or physical signal transmits through a cell as series of molecular events so the pathogen needs to intercept these molecular pathways at few positions to induce pathogenesis such as pathogen viability, infection or hypersensitivity. Results: The pathogen nodes of interception are not necessarily the most immunogenic; so that novel immunogenicity-improvement strategies need to be developed thought a chemical conjugation of the pathogen-carrier nodes to develop an efficient immune response in order to block pathogenesis. On the other hand, if pathogen-carriers are immunogens; toleration ought to be induced by this conjugation avoiding hypersensitivity. Thus, this paper addresses the biological plausibility of plant-phenolics as pathogen-carrier immunogenicity modulator haptens. Conclusion: The plant-phenolic compounds have in their structure functional groups such as hydroxyl, carbonyl, carboxyl, ester, or ether, capable of reacting with the amino or carbonyl groups of the amino acids of a pathogen-carrier to form conjugates. Besides, the varied carbon structures these phenolic compounds have; it is possible to alter the pathogen-carrier related factors that determine the immunogenicity: 1) Structural complexity, 2) Molecular size, 3) Structural heterogeneity, 4) Accessibility to antigenic determinants or epitopes, 5) Optical configuration, 6) Physical state, or 7) Molecular rigidity.

scholarly journals Analysis of miRNA-mRNA Crosstalk in Radiation-Induced Mouse Thymic Lymphomas to Identify miR-486 as a Critical Regulator by Targeting IGF2BP3 mRNA

2021 ◽  
Vol 10 ◽  
Author(s):  
Hainan Zhao ◽  
Suhe Dong ◽  
Jicong Du ◽  
Penglin Xia ◽  
Ruling Liu ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Target Genes ◽  
Environmental Carcinogens ◽  
Mice Model ◽  
Lymphoma Cells ◽  
Over Expression ◽  
Mirna Array ◽  
Radiation Induced ◽  
The Relationship

Ionizing radiation is one of the common environmental carcinogens. miRNAs play critical roles in the processes of tumor occurrence, development, metastasis. However, the relationship between radiation-induced carcinogenesis and miRNA rarely reported. This study is aimed to investigate the effect of miRNAs on radiation-induced carcinogenesis. In this study we established the radiation-induced thymic lymphoma mice model. By using miRNA array of RTL tissue and predicting for miRNAs target genes, a miRNA-mRNA crosstalk network was established. Based on this network, we identified a critical miRNA, miR-486, which was the most down-regulated in the radiation-induced carcinogenesis. Then the function of miR-486 was confirmed by using knockout mice and cellular experiments. As a result, miR-486 could inhibit proliferation of mouse lymphoma cells by targeting IGF2BP3 mRNA. The adenovirus over-expression miR-486 vector reduced tumorigenesis in vivo. MiR-486 knockout mice have a strong tendency of radiation-induced carcinogenesis. In conclusion, miR-486 inhibits the proliferation of lymphoma cells and tumorigenesis induced by radiation through targeting IGF2BP3.

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