amino acid

Overview

Amino acids are organic compounds carrying both an amine and a carboxylic acid group, and they are the building blocks of proteins. The 20 genetically encoded ones share a common plan: a central α-carbon bearing an amino group (–NH₂, except proline, whose nitrogen is enclosed in a ring and so is a secondary amine), a carboxyl group (–COOH), a hydrogen and a distinctive side chain that determines chemical identity. Only the L-stereoisomer is used in ribosomal synthesis, and at physiological pH the molecule exists as a zwitterion, the amine protonated and the carboxyl deprotonated. Two further residues, selenocysteine and pyrrolysine, are inserted co-translationally by recoding stop codons, and of the roughly 500 amino acids found in nature most are never incorporated into protein at all — including D-amino acids in bacterial cell walls and intermediates such as ornithine and citrulline. Nine of the 20 are essential in humans, meaning they cannot be synthesized and must come from diet.

Beyond building proteins, amino acids are metabolic hubs. Their carbon skeletons feed the tricarboxylic acid cycle as glucogenic or ketogenic substrates, while the nitrogen removed by transamination is disposed of through the urea cycle. Several are direct precursors of signaling molecules — arginine of nitric oxide, tryptophan of serotonin, tyrosine of catecholamines — and glycine and glutamate act as inhibitory and excitatory neurotransmitters in their own right. Leucine signals nutrient sufficiency to mTORC1, linking amino acid supply to growth.

Their distribution depends on dedicated transporters, including L-type amino acid transporter 1 (LAT1) and the neutral transporter SLC6A15 (B0AT2), which control passage across the blood-brain barrier and into tumors — LAT1 is exploited both by Cancers with high demand and by drugs designed to enter the brain disguised as amino acids. Inherited defects in their metabolism cause disease directly, as in phenylketonuria and maple syrup urine disease, and acquired dysregulation is implicated in preeclampsia, type 2 diabetes, metabolic dysfunction-associated steatotic liver disease and diabetic nephropathy, making amino acid profiles both biomarkers and therapeutic targets.

Recent Publications Summary

The publication list in the prompt is empty — the "Recent publications (title + abstract):" block contains no titles or abstracts, and the related-entities line says "None identified." There's nothing to synthesize from, and writing the section anyway would mean inventing studies and PMIDs.

Two likely causes on the generator side:

• No papers matched "Amino Acids" as a Target for the Chemical category, so the abstract-fetch step returned an empty set.
• The papers were found but the abstract text wasn't interpolated into the prompt template.

Given the working tree has scripts/makewiki.py modified and recent commits touching the Focus/recent-papers section logic, the second is worth checking first.

Send me the titles + abstracts (with PMIDs) and I'll write the 2–5 paragraph section immediately. Or, if you want, I can look at scripts/makewiki.py to find why the block came through empty.

What Changes, What Holds

1. No new evidence can be synthesized from an empty publication block
METHOD The recent-work section contributes no usable findings, so it does not alter the established account of amino acids at all. The immediate implication is procedural rather than biological: the article cannot be updated from this prompt because no titles, abstracts, or PMIDs are present to support a claim. That leaves the baseline unchanged and the evidence gap unresolved.

2. The missing abstracts point to a prompt-generation failure, not a biological result
METHOD The new information shifts attention to the pipeline that assembles recent literature, because the absence of papers may reflect either failed target matching or failed abstract interpolation. That matters for article maintenance, but it does not add or subtract from what is known about amino acids themselves. The established roles in protein synthesis, metabolism, and signaling remain intact; what changes is confidence in the completeness of the literature feed.

3. The empty recent-papers block should be debugged before any content update is attempted
METHOD The working-tree note makes the likely source of the omission a software issue worth checking first, which is a workflow concern rather than a scientific one. Nothing here revises amino acid biology, transport, or disease associations; instead, it suggests the article-generation process may be suppressing valid recent studies. Until that is fixed, the overview should not be expanded on the basis of this prompt.

4. The article cannot be updated until the missing titles and abstracts are supplied
METHOD The request for PMIDs and abstracts confirms that no evidence-based synthesis is currently possible, and the offer to inspect the script underscores that the problem may be upstream of the writing step. For the amino acid entry, this means the baseline stands as written and no new role, harm, or refinement is established. The only actionable change is to recover the missing literature feed or repair the extraction logic.

Overview update candidates: none.