glgB curation notes

• Q88FN1 is a reviewed 1,4-alpha-glucan branching enzyme (EC 2.4.1.18) that transfers an alpha-1,4-glucan segment to create an alpha-1,6 branch. [file:PSEPK/glgB/glgB-uniprot.txt, "Reaction=Transfers a segment of a (1->4)-alpha-D-glucan chain to a"]
• The reviewed pathway field assigns glycogen biosynthesis. This supports participation in polymer branching, not the TreSB precursor or GlgE elongation reactions. [file:PSEPK/glgB/glgB-uniprot.txt, "PATHWAY: Glycan biosynthesis; glycogen biosynthesis."]
• GH13 family membership does not make the net GlgB reaction hydrolytic. The GO:0004553 InterPro mapping was removed in favor of GO:0003844. [file:PSEPK/glgB/glgB-uniprot.txt, "Belongs to the glycosyl hydrolase 13 family. GlgB"] [file:PSEPK/glgB/glgB-uniprot.txt, "DR GO; GO:0003844; F:1,4-alpha-glucan branching enzyme activity"]
• Local PANTHER data place Q88FN1 in PTHR43651:SF3, specifically named 1,4-alpha-glucan branching enzyme. [file:interpro/panther/PTHR43651/PTHR43651-entries.csv, "Q88FN1"]
• PAINT places GO:0003844 at PTHR43651 ancestral node PTN000040010 using experimentally annotated branching enzymes, including the same-subfamily Mycobacterium exemplar P9WN45. [file:interpro/panther/PTHR43651/PTHR43651-paint.tsv, "PTN000040010"]
• Mycobacterium experiments identify GlgB as the fourth member of the TreS-Mak-GlgE-GlgB pathway but do not directly assay Q88FN1. PMID:20305657
• In KT2440, glucose-starvation transcriptomics directly reports upregulation of glgB with glycogen-biosynthesis genes, supporting its physiological carbon-storage context without independently determining the enzyme reaction. PMID:32267616
• GO:0043169 cation binding is marked over-annotated: the InterPro mapping specifies neither ion nor site, and the reviewed UniProt record contains no cofactor or cation-binding feature.

OpenScientist reconciliation

Source: file:PSEPK/glgB/glgB-deep-research-openscientist.md (1,461.43 seconds).

• The report corroborates the GH13 GlgB identity, alpha-1,6 branch-forming role,
  and placement downstream of TreSB and GlgE.
• Its proposed catalytic-residue positions, operon inference, and GlgC-absence
  interpretation are computational hypotheses rather than direct Q88FN1
  evidence and were not promoted into the curated core function.
• The report found no direct biochemical or genetic characterization of
  Q88FN1; the review therefore retains the target-specific UniProt and KT2440
  transcriptomic evidence as its primary grounding.