scholarly journals Endocytosis of exogenous GM1 ganglioside and cholera toxin by neuroblastoma cells.

1983 ◽  
Vol 3 (1) ◽  
pp. 91-101 ◽  
Author(s):  
N K Gonatas ◽  
A Stieber ◽  
J Gonatas ◽  
T Mommoi ◽  
P H Fishman
Keyword(s):  
Cholera Toxin ◽  
Neuroblastoma Cells ◽  
Double Labeling ◽  
Electron Microscope Autoradiography ◽  
Density Distributions ◽  
Quantitative Studies ◽  
Covalently Linked ◽  
The Relationship ◽  
Cytochemical Marker ◽  
In Cells

Cholera toxin (CT) covalently linked to horseradish peroxidase (HRP) is a specific cytochemical marker for its receptor, the monosialoganglioside GM1. The binding and endocytosis of exogenous [3H]GM1 by cultured murine neuroblastoma cells (line 2A [CCl-131] ), which contain predominantly GM3, was examined by quantitative electron microscope autoradiography. The relationship between exogenous receptor, [3H]GM1, and CT HRP was studied in double labeling experiments consisting of autoradiographic demonstration of [3H]GM1 and cytochemical visualization of HRP. Exogenous [3H]GM1 was not degraded after its endocytosis by cells for 2 h at 37 degrees C. Quantitative studies showed similar grain density distributions in cells treated with [3H]GM1 alone and in cells treated with [3H]GM1 followed by CT-HRP. Qualitative studies conducted in double labeling experiments showed autoradiographic grains over the peroxidase-stained plasma membrane, lysosomes, and vesicles at the trans aspect of the Golgi apparatus. The findings indicate that exogenous glycolipid is associated with the plasmid membrane of deficient cells and undergoes endocytosis. The quantitative ultra-structural autoradiographic studies are consistent with the hypothesis that the spontaneous endocytosis of exogenous [3H]GM1 controls the subsequent uptake of CT-HRP.

Endocytosis of exogenous GM1 ganglioside and cholera toxin by neuroblastoma cells

1983 ◽  
Vol 3 (1) ◽  
pp. 91-101
Author(s):  
N K Gonatas ◽  
A Stieber ◽  
J Gonatas ◽  
T Mommoi ◽  
P H Fishman
Keyword(s):  
Cholera Toxin ◽  
Neuroblastoma Cells ◽  
Double Labeling ◽  
Electron Microscope Autoradiography ◽  
Density Distributions ◽  
Quantitative Studies ◽  
Covalently Linked ◽  
The Relationship ◽  
Cytochemical Marker ◽  
In Cells

Cholera toxin (CT) covalently linked to horseradish peroxidase (HRP) is a specific cytochemical marker for its receptor, the monosialoganglioside GM1. The binding and endocytosis of exogenous [3H]GM1 by cultured murine neuroblastoma cells (line 2A [CCl-131] ), which contain predominantly GM3, was examined by quantitative electron microscope autoradiography. The relationship between exogenous receptor, [3H]GM1, and CT HRP was studied in double labeling experiments consisting of autoradiographic demonstration of [3H]GM1 and cytochemical visualization of HRP. Exogenous [3H]GM1 was not degraded after its endocytosis by cells for 2 h at 37 degrees C. Quantitative studies showed similar grain density distributions in cells treated with [3H]GM1 alone and in cells treated with [3H]GM1 followed by CT-HRP. Qualitative studies conducted in double labeling experiments showed autoradiographic grains over the peroxidase-stained plasma membrane, lysosomes, and vesicles at the trans aspect of the Golgi apparatus. The findings indicate that exogenous glycolipid is associated with the plasmid membrane of deficient cells and undergoes endocytosis. The quantitative ultra-structural autoradiographic studies are consistent with the hypothesis that the spontaneous endocytosis of exogenous [3H]GM1 controls the subsequent uptake of CT-HRP.

scholarly journals Endocytosis of cholera toxin in GERL-like structures of murine neuroblastoma cells pretreated with GM1 ganglioside. Cholera toxin internalization into Neuroblastoma GERL.

1979 ◽  
Vol 81 (3) ◽  
pp. 543-554 ◽  
Author(s):  
K C Joseph ◽  
A Stieber ◽  
N K Gonatas
Keyword(s):  
Golgi Apparatus ◽  
Horseradish Peroxidase ◽  
Cholera Toxin ◽  
Plasma Membranes ◽  
Neuroblastoma Cells ◽  
Gm1 Ganglioside ◽  
Murine Neuroblastoma ◽  
Positive Elements ◽  
Subunit B ◽  
Cytochemical Marker

Cholera toxin (CT), covalently attached to horseradish peroxidase (HRP), is a specific cytochemical marker for GM1 ganglioside (GM1) and retains the ability of the native toxin to raise levels of cyclic AMP in avian erythrocytes. Using a cytochemical stain for HRP, we found that 9% of control cultured murine neuroblastoma cells bound cholera toxin-horseradish peroxidase conjugates (CT-HRP) on their surfaces after incubations for 1 h at 4 degrees C. Exogenous GM1, the natural receptor of CT, becomes associated in the culture medium with the plasma membranes of these cells so that 96% of cells are stained. Cells preincubated with GM1 at 4 degrees C were exposed to CT-HRP for 1 h at 4 degrees C. After washing, cells were incubated at 37 degrees C for 30 min-24 h. Endocytosis of CT-HRP occurred within 30 min and CT-HRP remained, throughout the 24-h period, in tubules, vesicles, and cisternae often found near the Golgi apparatus; this aggregate of peroxidase-positive elements probably corresponds to Golgi apparatus-endoplasmic reticulum-lysosomes (GERL) of neurons. In metaphase cells, CT-HRP was observed in aggregates of vesicles and tubules clustered near the centriole. Conjugates of HRP with subunit B, the GM1 binding component of CT, were internalized by cells pretreated with GM1 as was CT-HRP. The 9% of neuroblastoma cells binding CT-HRP in the absence of exogenous GM1 internalized the ligand in a manner indistinguishable from that of the treated cells. These findings indicate that, in neuroblastoma cells, a system of vesicles, tubules, and cisternae, analogous to GERL of neurons, is the primary recipient of adsorptive endocytosis of CT bound to endogenous or exogenously introduced GM1.

Cholera toxin covalently linked with horseradish peroxidase does not activate the adenylate cyclase of neuroblastoma cells

1982 ◽  
Vol 137 (2) ◽  
pp. 449-452 ◽  
Author(s):  
Frixos C. Charalampous ◽  
Jacqueline O. Gonatas ◽  
Simon Van Heyningen ◽  
Nicholas K. Gonatas
Keyword(s):  
Horseradish Peroxidase ◽  
Adenylate Cyclase ◽  
Cholera Toxin ◽  
Neuroblastoma Cells ◽  
Covalently Linked

A Phenomenological Theory of Socioeconomic Systems with Spatial Interactions

1982 ◽  
Vol 14 (7) ◽  
pp. 869-888 ◽  
Author(s):  
P F Lesse
Keyword(s):  
Lagrange Multipliers ◽  
Average Cost ◽  
Phenomenological Theory ◽  
Traffic Flows ◽  
Spatial Interactions ◽  
Practical Application ◽  
Density Distributions ◽  
Expected Values ◽  
Probability Density Distributions ◽  
The Relationship

This paper deals with a class of models which describe spatial interactions and are based on Jaynes's principle. The variables entering these models can be partitioned in four groups: (a) probability density distributions (for example, relative traffic flows), (b) expected values (average cost of travel), (c) their duals (Lagrange multipliers, traffic impedance coefficient), and (d) operators transforming probabilities into expected values. The paper presents several dual formulations replacing the problem of maximizing entropy in terms of the group of variables (a) by equivalent extreme problems involving groups (b)-(d). These problems form the basis of a phenomenological theory. The theory makes it possible to derive useful relationships among groups (b) and (c). There are two topics discussed: (1) practical application of the theory (with examples), (2) the relationship between socioeconomic modelling and statistical mechanics.

Rhodamine isothiocyanate coupled peanut lectin for quantitative studies of D-galactosyl receptors of neuroblastoma cells

1981 ◽  
Vol 37 (11) ◽  
pp. 1154-1157 ◽  
Author(s):  
M. Caron ◽  
M. -A. Deugnier ◽  
X. Albe ◽  
J. -C. Bisconte ◽  
A. Faure
Keyword(s):  
Neuroblastoma Cells ◽  
Peanut Lectin ◽  
Quantitative Studies ◽  
Rhodamine Isothiocyanate

scholarly journals Posttranslational Regulation of IL-23 Production Distinguishes the Innate Immune Responses to Live Toxigenic versus Heat-Inactivated Vibrio cholerae

mSphere ◽  
2019 ◽  
Vol 4 (4) ◽  
Author(s):  
Ana A. Weil ◽  
Crystal N. Ellis ◽  
Meti D. Debela ◽  
Taufiqur R. Bhuiyan ◽  
Rasheduzzaman Rashu ◽  
...  
Keyword(s):  
Immune Responses ◽  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Protective Immunity ◽  
Innate Immune ◽  
Posttranslational Regulation ◽  
Content Type ◽  
In Cells ◽  
Cholera Vaccines

ABSTRACT Vibrio cholerae infection provides long-lasting protective immunity, while oral, inactivated cholera vaccines (OCV) result in more-limited protection. To identify characteristics of the innate immune response that may distinguish natural V. cholerae infection from OCV, we stimulated differentiated, macrophage-like THP-1 cells with live versus heat-inactivated V. cholerae with and without endogenous or exogenous cholera holotoxin (CT). Interleukin 23A gene (IL23A) expression was higher in cells exposed to live V. cholerae than in cells exposed to inactivated organisms (mean change, 38-fold; 95% confidence interval [95% CI], 4.0 to 42; P < 0.01). IL-23 secretion was also higher in cells exposed to live V. cholerae than in cells exposed to inactivated V. cholerae (mean change, 5.6-fold; 95% CI, 4.4 to 11; P < 0.001). This increase in IL-23 secretion was more marked than for other key innate immune cytokines (e.g., IL-1β and IL-6) and dependent on exposure to the combination of both live V. cholerae and CT. While IL-23 secretion was reduced following stimulation with either heat-inactivated wild-type V. cholerae or a live isogenic ctxAB mutant of V. cholerae, the addition of exogenous CT restored IL-23 secretion in combination with the live isogenic ctxAB mutant V. cholerae, but not when it was paired with stimulation by heat-inactivated V. cholerae. The posttranslational regulation of IL-23 under these conditions was dependent on the activity of the cysteine protease cathepsin B. In humans, IL-23 promotes the differentiation of Th17 cells to T follicular helper cells, which maintain and support long-term memory B cell generation after infection. Based on these findings, the stimulation of IL-23 production may be a determinant of protective immunity following V. cholerae infection. IMPORTANCE An episode of cholera provides better protection against reinfection than oral cholera vaccines, and the reasons for this are still under study. To better understand this, we compared the immune responses of human cells exposed to live Vibrio cholerae with those of cells exposed to heat-killed V. cholerae (similar to the contents of oral cholera vaccines). We also compared the effects of active cholera toxin and the inactive cholera toxin B subunit (which is included in some cholera vaccines). One key immune signaling molecule, IL-23, was uniquely produced in response to the combination of live bacteria and active cholera holotoxin. Stimulation with V. cholerae that did not produce the active toxin or was killed did not produce an IL-23 response. The stimulation of IL-23 production by cholera toxin-producing V. cholerae may be important in conferring long-term immunity after cholera.

scholarly journals Nitrate Accumulation in Relation to Molybdenum Deficiency Leaf Scorch Symptoms

1960 ◽  
Vol 13 (1) ◽  
pp. 104
Author(s):  
LF Notley ◽  
GL Wilson
Keyword(s):  
Leaf Tissue ◽  
Nitrate Content ◽  
Nitrate Accumulation ◽  
Leaf Scorch ◽  
Quantitative Studies ◽  
The Relationship

The accumulation of nitrate in the leaf tissue of nitrate-supplied, molybdenumdeficient plants has been suspected as a cause of the scorching symptoms which frequently develop (e.g. Agarwala 1952; Agarwala and Hewitt 1952; Hewitt and McCready 1953). Quantitative studies of the relationship between nitrate content and the symptoms have, however, been inconclusive. The literature suggests (cf. Wilson and Waring 1948; Johnson, Pearson, and Stout 1952) that this may follow from the estimation of nitrate in whole leaf tissue rather than in damaged portions.

scholarly journals Heat Stress Modulates the GSK-3β Levels and Tau Phosphorylation

2020 ◽  
Author(s):  
Tushar Dubey ◽  
Subashchandrabose Chinnathambi
Keyword(s):  
Heat Stress ◽  
High Temperature ◽  
Posttranslational Modifications ◽  
Neuroblastoma Cells ◽  
Tau Phosphorylation ◽  
Pathological State ◽  
Progressive Dementia ◽  
Stressed Cells ◽  
Gsk 3Β ◽  
In Cells

Alzheimer&rsquo;s disease is a prominent neurological disorder, which leads to progressive dementia. The microtubule-associated protein Tau is been considered as one of the major causes of Alzheimer&rsquo;s disease. Physiologically Tau assists in the stabilization of microtubules, contrary to this the pathological state of Tau results in the formation of neurotoxic tangles of Tau. The posttranslational modifications, such as GSK-3&beta;-mediated Tau phosphorylation results in the generation of Tau pathology. Neuroinflammation generated in Alzheimer&rsquo;s disease, contributes to elevated body temperature. The aim of present work is to study the effect of high temperature on Tau phosphorylation. The neuroblastoma cells were exposed to heat stress for 40 minutes. The immunofluorescence and western blot studies suggested that high temperature increases the levels of GSK-3&beta; in cells. Heat stressed cells was also observed to have elevated levels of phosphorylated Tau. Additionally, heat stressed cells found to have modulated nuclear transport as the level of Ran was reduced. The results of present work suggested that increased temperature could be considered as a risk factor in Alzheimer&rsquo;s disease as it elevated the GSK-3&beta; levels in cells thus, resulting in increased Tau phosphorylation.

Sign in / Sign up

Export Citation Format

Share Document