GPCR Map- "neutralization of the antibodies (acquired variably against G-PCR structures) caused an immediate easing of LCS (long covid syndrome) and CFS (chronic fatigue syndrome) symptoms

[Joseph Arabasz MD]

Subject- GPCR Map "neutralization of the antibodies (acquired variably against G-PCR structures) caused an immediate easing of LCS (long covid syndrome) and CFS (chronic fatigue syndrome) symptoms

Dear Topica,

                                                                                                                                                                                                                                        I hope this note finds You well

     Puppy Chiquita Auditory Service Animal is now with the Ages

      

excerpted from Berlin Cures Articles-

"BC7 aptamer studies-

The purpose of B7 aptamer was to eliminate AAbs (aka SELF ANTIBODIES) against GPCR-AAbs (G-Protein Coupled Receptor Antibodies), and to improve the impaired capillary microcirculation of the glaucoma Patients, measured by OCT-A Research Lab device

(Optical Coherence Tomography Angiography)

     As mentioned before, felt that some antibodies which disrupt the G-Protein Coupled Receptor (G-PCR) on the external side of the cell, could be acquired

     There is at least single type of antibody which is acquired from another disease process which causes problems on the G-Protein Couple Receptor which transmits signals from the external cellular wall to the cytoplasm and there might be others of that type

     eg, adrenaline doesn't enter the cell

But adrenaline attaches to the G-Protein Couple Receptor on the external side of the cell

     The G-PC Receptor then re-configures itself and that transfers the signal to the cell

     The severe covid long haul symptoms acquired after that disease would imply there are others antibodies against the G-Protein Coupled Receptors which occur secondarily after other diseases

to be continued

Best wishes always

Thank You for Your assistance with this matter

Cordially,

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Introduction

G protein-coupled receptors (GPCRs) represent the largest protein group encoded by the human genome. Located on the cell membrane, they transduce extracellular signals into key physiological effects.1 Their endogenous ligands include odors, hormones, neurotransmitters, chemokines, etc., varying from photons, amines, carbohydrates, lipids, peptides to proteins. GPCRs have been implicated in a large number of diseases, such as type 2 diabetes mellitus (T2DM), obesity, depression, cancer, Alzheimer’s disease, and many others.2 Activated by external signals through coupling to different G proteins or arrestins, GPCRs elicit cyclic adenosine 3,5-monophosphate (cAMP) response, calcium mobilization, or phosphorylation of extracellular regulated protein kinases 1/2 (pERK1/2).3 The seven-transmembrane protein property endows them easy to access, while the diversified downstream signaling pathways make them attractive for drug development.4 The human GPCR group is divided into classes A (rhodopsin), B (secretin and adhesion), C (glutamate), and F (Frizzled) subfamilies according to their amino acid sequences (Fig. 1). Of the 826 human GPCRs, approximately 350 non-olfactory members are regarded as sites for possible medicines and 165 of them are validated drug sites (Fig. 1 and Table S1).4,5,6 Latest statistical data indicate that 527 Food and Drug Administration (FDA)-approved drugs4 and ∼60 drug candidates currently in clinical trials attach GPCRs (Table S1).5

Fig. 1

Phylogenetic tree of GPCRs as drug sites. Node represents GPCR named according to its gene name. Receptors with approved drugs on the market are highlighted by color. GPCRs are organized according to GPCR database.4 Approved drug list was derived from previous publications,4,11 complemented by additional search of newly approved entities at Drugs@FDA (accessdata.fda.gov) until June 2020.