Thiamine
Metalloenzyme

Triphosphate Tunnel Metalloenzyme Function in Senescence Highlights a Biological Diversification of This Protein Superfamily

https://academic.oup.com/plphys/article/175/1/473/6117054?login=false

The triphosphate tunnel metalloenzyme (TTM) superfamily comprises a group of enzymes that hydrolyze organophosphate substrates. They exist in all domains of life, yet the biological role of most family members is unclear.

AtTTM2 displays pyrophosphatase activity and is involved in pathogen resistance.

..

Thiamine triphosphatase and the CYTH superfamily of proteins

https://febs.onlinelibrary.wiley.com/doi/full/10.1111/febs.12498

Members of this superfamily of proteins exist in all organisms, including bacteria, archaeons, fungi, plants, and animals (except birds), and can be traced back to the last universal common ancestor. Their sequences include several charged residues involved in divalent cation and triphosphate binding.

..

Phase separation of a yeast prion protein promotes cellular fitness

https://www.science.org/doi/10.1126/science.aao5654

..

Polyphosphate

TTPase
Thiamin Triphosphatase

GTPase
Guanosine Triphosphatase

..

Prion propagation and inositol polyphosphates

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5949079/

The first report of genetic variations in the chicken prion protein gene

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6277184/

To date, spontaneous prion disease in birds has not been reported, and parenteral and oral challenge of prion agent has failed to infected chickens. Thus, several studies have attempted to find the feature of the chicken prion protein that leads to prion disease resistance.

Octapeptide repeat sequence was found only in mammals. Chicken has a significantly different form of tandem repeat, called Hexapeptide repeat (amino acids, peptide, protein).

..

Hexapeptide
Acetyl Hexapeptide-8 Amide
Botulinum
[Birds]

https://en.m.wikipedia.org/wiki/Acetyl_hexapeptide-3

Octapeptide
Ace
Angiotensin II
[Mammals]

Angiotensin-converting enzyme, or ACE, is a central component of the renin–angiotensin system (RAS).

https://en.m.wikipedia.org/wiki/Angiotensin-converting_enzyme

..

both Hexapeptide & Octapeptide are used in skin products as botulinum Botox?

the location that defines Piron resistance or pathogenic, is a botox pathway?

its interesting that the Prion pathway went straight to Octapeptide = ACE, precursor to ACE II.

HIV has ACE II inserts? why is Prion in the same pathways?

this is an incomplete story, specially regarding protein metabolite disfunction & and thiamine for carbon metabolite disfunction.

Urea Cycle
Steps of Urea Cycle
Citrulline
Urea Cycle Disorders

..

Octapeptide
Angiotensin-Converting Enzyme ACE
Prion

The Effect of Octapeptide Repeats on Prion Folding and Misfolding

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7918816/

The Number of Octapeptide Repeats Affects the Structure and the Thermal Stability of Prion Proteins

The Expansion Rather Than the Deletion of Octapeptides Enhances the Kinetics of Fibril Conversion

The Number of Octapeptide Repeats Affects the Structures of Fibrils

The Number of Octapeptide Repeats Affects the Cytotoxicity of the Amyloid Fibrils

..

Thiamine Triphosphate

https://en.m.wikipedia.org/wiki/Thiamine_triphosphate

In E. coli, ThTP is accumulated in the presence of glucose during amino acid starvation. On the other hand, suppression of the carbon source leads to the accumulation, of adenosine thiamine triphosphate (AThTP).

Adenosine Thiamine Triphosphate

https://en.m.wikipedia.org/wiki/Adenosine_thiamine_triphosphate

The molecule is made up of thiamine and adenosine joined together with phosphate groups. It is similar in structure to NAD+. The function of AThTP is not currently known but it has been shown to inhibit the activity of PARP-1.

PARP1

https://en.m.wikipedia.org/wiki/PARP1

Following severe DNA damage, excessive activation of PARP1 can lead to cell death. Initially, overactivation of the enzyme was linked to apoptotic cell death but later, PARP1-mediated cell death turned out to show characteristics of necrotic cell death (i.e. early plasma membrane disruption, structural and functional mitochondrial alterations).