Redemption - Lawful Money

I really enjoyed today's Tuesday Zoom call. At around the fourteen minute mark Carrie's guest made a remark about paying taxes to a government that kills our children? There is only one way around paying the income tax that is supported by law. I make a reference to this lawful money redemption in another thread here:

drive.google.com

Here is an example of a suitor who got all his withholdings refunded:

http://savingtosuitorsclub.net/showthread.php?2721-Greetings!!&p=27259&viewfull=1#post27259

$213,093.79 refunded? Well, you might not have that much withheld from your paychecks.

Here is how it works.

You do not want the IRS to make any calculations so you make your demand starting now, but wait until you have a full year under demand for lawful money. So you would work like usual through 2023 and then claim all your withholdings back in early 2024. At that time you would declare EXEMPT on the W-4 Form because you owed no tax for 2023 and are expecting to owe none in 2024. From then on, you simply report through the 1040 Form so that the IRS will not calculate your refund for you based on reporting like W-2 and 1099.

If you find a 30% pay raise interesting get a look at www.lawfulmoneytrust.com and change your life. The money is only a model of redemption. It is redeeming your mind from central banking delusions about debt that really matters.

The later topic was really fascinating, about the Sythians and Khazarians. I read a couple books by Arthur KOESTLER about this. The guest speaker was talking about gene K26R being resilient to shedding? I want to hear more!

2B58

SSAT with coa_sp, spermine disordered, K26R mutant

• PDB DOI: 10.2210/pdb2B58/pdb

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• PubMed Abstract:
  

www.rcsb.org

SSAT with coa_sp, spermine disordered, K26R mutant

Spermidine/spermine N1-acetyltransferase (SSAT) is a key enzyme in the control of polyamine levels in human cells, as acetylation of spermidine and spermine triggers export or degradation. Increased intracellular polyamine levels accompany several types of cancers as well as other human diseases, and compounds that affect the expression, activity, or stability of SSAT are being explored as potential therapeutic drugs. We have expressed human SSAT from the cloned cDNA in Escherichia coli and have determined high-resolution structures of wild-type and mutant SSAT, as the free dimer and in binary and ternary complexes with CoA, acetyl-CoA (AcCoA), spermine, and the inhibitor N1,N11bis-(ethyl)-norspermine (BE-3-3-3). These structures show details of binding sites for cofactor, substrates, and inhibitor and provide a framework to understand enzymatic activity, mutations, and the action of potential drugs. Two dimer conformations were observed: a symmetric form with two open surface channels capable of binding substrate or cofactor, and an asymmetric form in which only one of the surface channels appears capable of binding and acetylating polyamines. SSAT was found to self-acetylate lysine-26 in the presence of AcCoA and absence of substrate, a reaction apparently catalzyed by AcCoA bound in the second channel of the asymmetric dimer. These unexpected and intriguing complexities seem likely to have some as yet undefined role in regulating SSAT activity or stability as a part of polyamine homeostasis. Sequence signatures group SSAT with proteins that appear to have thialysine Nepsilon-acetyltransferase activity.

drive.google.com