Identification of somatic hybrids in plant protoplast fusions with monoclonal antibodies to plasma-membrane antigens

Planta ◽  
1987 ◽  
Vol 170 (1) ◽  
pp. 49-54 ◽  
Author(s):  
M. S. Fitter ◽  
P. M. Norman ◽  
M. G. Hahn ◽  
V. P. M. Wingate ◽  
C. J. Lamb
Keyword(s):  
Monoclonal Antibodies ◽  
Plasma Membrane ◽  
Somatic Hybrids ◽  
Plant Protoplast ◽  
Membrane Antigens

scholarly journals Monoclonal antibodies that immunoreact with a cation-stimulated plant membrane ATPase

1982 ◽  
Vol 203 (1) ◽  
pp. 51-54 ◽  
Author(s):  
J J C Chin
Keyword(s):  
Monoclonal Antibody ◽  
Monoclonal Antibodies ◽  
Plasma Membrane ◽  
Marker Enzyme ◽  
Membrane Atpase ◽  
Hybridoma Technology ◽  
Membrane Antigens ◽  
Monospecific Antibodies

Hybridoma technology has been used successfully to generate monoclonal-antibody probes against protoplast membrane antigens. Hybridomas secreting monoclonal antibodies that either inhibit or stimulate a putative plasma-membrane marker enzyme, (K+ + Mg2+)-stimulated pH 6.5 ATPase, have been identified and cloned. The specificity of monoclonal-antibody probes on the activity of other phosphate-hydrolysing enzymes has also been examined. The production and identification of monospecific antibodies capable of immunoreacting with particular component proteins in a complex plant membrane mixture highlight the usefulness of hybridoma methodology for the enzymologist, especially since such monoclonal antibodies can be used in the purification of proteins by immunoaffinity techniques.

Monoclonal antibodies to plant plasma-membrane antigens

Planta ◽  
1986 ◽  
Vol 167 (4) ◽  
pp. 452-459 ◽  
Author(s):  
P. M. Norman ◽  
V. P. M. Wingate ◽  
M. S. Fitter ◽  
C. J. Lamb
Keyword(s):  
Monoclonal Antibodies ◽  
Plasma Membrane ◽  
Membrane Antigens ◽  
Plant Plasma Membrane

NEUROBLASTOMA IMMUNOTHERAPY

2019 ◽  
Vol 65 (2) ◽  
pp. 181-187
Author(s):  
Aleksandr Druy ◽  
Svetlana Kuleva
Keyword(s):  
T Cells ◽  
Monoclonal Antibodies ◽  
High Risk ◽  
Checkpoint Inhibitors ◽  
Innate And Adaptive Immunity ◽  
Car T Cells ◽  
Car T ◽  
Membrane Antigens ◽  
Theoretical Evidence ◽  
Blocking Antibodies

The recent data about innate and adaptive immunity against neuroblastoma are described in the article. The era of neuroblastoma immunotherapy started since the evidence of anti-GD2 monoclonal antibodies efficiency. Nowadays monoclonal antibodies against GD2 are introduced into schemes of maintenance therapy for high-risk neuroblastoma patients. Developing of T-cells expressing chimeric antigen receptor (CAR-T cells) directed to membrane antigens is the perspective of neuroblastoma immunotherapy. PD1/PD-L1 blocking antibodies as immune checkpoint inhibitors have the theoretical evidence of potential effectiveness. Application of immunotherapeutic approaches in high-risk neuroblastoma patients together with conventional multimodal therapies requires further investigation.

Enzyme-linked immunosorbent assay of autoantibodies reacting with thyroid plasma membrane antigens in sera of patients with autoimmune thyroid diseases

1986 ◽  
Vol 113 (2) ◽  
pp. 255-260 ◽  
Author(s):  
Andrzej Gardas ◽  
Kathleen L. Rives
Keyword(s):  
Plasma Membrane ◽  
Immunosorbent Assay ◽  
Lupus Erythematosus ◽  
Antithyroid Drug ◽  
Cross Reactivity ◽  
Enzyme Linked Immunosorbent Assay ◽  
Autoimmune Thyroid Diseases ◽  
Nodular Goitre ◽  
Membrane Antigens ◽  
Toxic Nodular Goitre

Abstract. A sensitive and specific enzyme-linked immunosorbent assay (ELISA) for the detection of autoantibodies reacting with thyroid plasma membrane antigens has been established. Autoantibodies reacting with thyroid plasma membrane antigens were detected by the ELISA in 95% of untreated hyperthyroid Graves', 68% of antithyroid drug-treated Graves' up to four months of the therapy, in 62% of Hashimoto's thyroiditis and in 8.9% of toxic nodular goitre. The ELISA was negative in 100% healthy blood donors, 100% non-toxic nodular goitre, in 12 patients with rheumatoid arthritis, 18 patients with scleroderma and 94% of patients with systemic lupus erythematosus. The mean value of autoantibodies titre was higher in untreated hyperthyroid Graves' (1:84 000) and lowest in positive patients with autoimmune disease of non-thyroid origin (1:4000). The cross-reactivity of antimicrosomal antigen antibodies was below 10%; there was no influence of antithyroglobulin antibodies on the ELISA; and most of the autoantibodies react with plasma membrane antigens different from the TSH binding sites.

Profilin is predominantly associated with monomeric actin in Acanthamoeba

1999 ◽  
Vol 112 (21) ◽  
pp. 3779-3790 ◽  
Author(s):  
D.A. Kaiser ◽  
V.K. Vinson ◽  
D.B. Murphy ◽  
T.D. Pollard
Keyword(s):  
Monoclonal Antibodies ◽  
Plasma Membrane ◽  
Fluorescent Antibody ◽  
Gel Filtration ◽  
Live Cells ◽  
A431 Cells ◽  
Antibody Staining ◽  
Large Particles ◽  
Biochemical Fractionation ◽  
Fluorescent Antibody Staining

We used biochemical fractionation, immunoassays and microscopy of live and fixed Acanthamoeba to determine how much profilin is bound to its known ligands: actin, membrane PIP(2), Arp2/3 complex and polyproline sequences. Virtually all profilin is soluble after gentle homogenization of cells. During gel filtration of extracts on Sephadex G75, approximately 60% of profilin chromatographs with monomeric actin, 40% is free and none voids with Arp2/3 complex or other large particles. Selective monoclonal antibodies confirm that most of the profilin is bound to actin: 65% in extract immunoadsorption assays and 74–89% by fluorescent antibody staining. Other than monomeric actin, no major profilin ligands are detected in crude extracts. Profilin-II labeled with rhodamine on cysteine at position 58 retains its affinity for actin, PIP(2) and poly-L-proline. When syringe-loaded into live cells, it distributes throughout the cytoplasm, is excluded from membrane-bounded organelles, and concentrates in lamellapodia and sites of endocytosis but not directly on the plasma membrane. Some profilin fluorescence appears punctate, but since no particulate profilin is detected biochemically, these spots may be soluble profilin between organelles that exclude profilin. The distribution of profilin in fixed human A431 cells is similar to that in amoebas. Our results show that the major pool of polymerizable actin monomers is complexed with profilin and spread throughout the cytoplasm.

scholarly journals Regulated expression of CD36 during monocyte-to-macrophage differentiation: potential role of CD36 in foam cell formation

Blood ◽  
1996 ◽  
Vol 87 (5) ◽  
pp. 2020-2028 ◽  
Author(s):  
HY Huh ◽  
SF Pearce ◽  
LM Yesner ◽  
JL Schindler ◽  
RL Silverstein
Keyword(s):  
Monoclonal Antibodies ◽  
Plasma Membrane ◽  
Foam Cell ◽  
Cell Formation ◽  
Foam Cell Formation ◽  
Mrna Levels ◽  
Macrophage Differentiation ◽  
Differentiation Potential ◽  
Intracellular Pool

Abstract CD36 is an 88-kD integral membrane glycoprotein expressed on monocytes, platelets, and certain microvascular endothelium serving distinct cellular functions both as an adhesive receptor for thrombospondin, collagen, and Plasmodium falciparum-infected erythrocytes, and as a scavenger receptor for oxidized low-density lipoprotein and apoptotic neutrophils. In this study, we examined the expression of CD36 during in vitro differentiation of peripheral blood monocytes into culture- derived macrophages. Steady-state mRNA levels of CD36 showed a transient eightfold increase during monocyte-to-macrophage differentiation, peaking at the early macrophage stage (days 3 or 4 in culture), following a gradual decrease back to baseline levels by the mature macrophage stage (days 7 or 8 in culture). Immunoblotting with monoclonal antibodies to CD36 supported this transient, yet significant (8- to 10-fold) increase in total protein levels of CD36. The increased CD36 protein was observed at the plasma membrane, whereas an intracellular pool of CD36 was also detected from day 2 to day 6 in culture through indirect immunofluorescence. A concomitant twofold increase in the cells' ability to bind 125I-thrombospondin at the early macrophage stage (day 4) verified the functional competency of the plasma membrane localized CD36, and supported the presence of an intracellular pool of CD36. The in vitro differentiated macrophages as well as alveolar macrophages remained responsive to macrophage colony- stimulating factor (M-CSF), a known transcriptional regulator of monocyte CD36. The M-CSF-induced macrophages resulted in enhanced foam cell formation, which was inhibitable with monoclonal antibodies to CD36. Thus, the transient expression of CD36 during monocyte-to- macrophage differentiation, and the ability of M-CSF to maintain macrophage CD36 at elevated levels, may serve as a critical process in dictating the functional activity of CD36 during inflammatory responses and atherogenesis.

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