Rbpj (mouse) review notes

UniProt P31266 (SUH_MOUSE), Recombining binding protein suppressor of hairless (RBP-Jkappa, CSL/CBF1),
526 aa. PANTHER PTHR10665 (RECOMBINING BINDING PROTEIN SUPPRESSOR OF HAIRLESS). MGI:96522.
Notch-module role: CSL — the DNA-binding nuclear effector of canonical Notch signalling.

Molecular function

• Sequence-specific DNA-binding TF (CGTGGGAA)
  PMID:8749394
• Binds the Notch1 intracellular RAM domain directly
  PMID:8749394
• Interacts with all four mouse Notch proteins (as opposed to paralog RBP-L/Rbpjl)
  PMID:9111338
• Repressor-to-activator switch; RAM binding creates Mastermind docking site
  PMID:18381292
• Repression in absence of NICD through corepressors (SHARP/CtIP/CtBP, KyoT2, L3MBTL3-KDM1A)
  PMID:16287852
  PMID:24290140
  PMID:29030483
• Notch-independent role: component of PTF1-J trimeric complex with Ptf1a/E-protein in early pancreas
  PMID:17938243
  Later replaced by the pancreas-restricted paralog Rbpjl (constitutively active, Notch-independent).
• Baf60c stabilises NICD-RBP-J interactions PMID:17210915.

Biological process

• Required for essentially all canonical Notch signalling; knockout phenocopies Notch1 null
  PMID:8749394
• Direct Notch target enhancers contain RBP-J sites, e.g. Nodal node enhancer PMID:12730124.
• Many developmental IMP annotations (heart, vasculature, somitogenesis, skin, immune cells, testis,
  pancreas, etc.) reflect loss of Notch signalling in those tissues: pleiotropic consequences, kept as
  non-core.

Pathway-variant relevance

• Mammals have one CSL (Rbpj) + tissue-restricted paralog Rbpjl (lung/pancreas) that does not bind Notch
  PMID:9111338. Rbpj also functions Notch-independently in PTF1-J.
• Zebrafish has rbpja/rbpjb; Drosophila Su(H); C. elegans lag-1.

Deep research

Falcon deep research completed (Rbpj-deep-research-falcon.md; wrapper reported a 600 s timeout but the
falcon client finished and wrote the file). Consistent with the above
[file:mouse/Rbpj/Rbpj-deep-research-falcon.md "Rbpj encodes a sequence-specific DNA-binding transcription factor that serves as the central nuclear mediator of canonical Notch signaling in mammals"].

2026-10-12 Ortholog/family audit (Dll1, Dll3, Hes7, Rbpj)

• GOA refreshed: no new rows, coverage complete. Compared with human RBPJ and worm lag-1.
• Core functions agree. All three have DNA-binding TF activity (GO:0000981), Pol II cis-regulatory sequence-specific DNA binding, positive regulation of transcription of Notch receptor target (GO:0007221) and the CSL-Notch-Mastermind complex. The Notch binding core MF matches lag-1. Human RBPJ has no Notch binding row in GOA.
• Changed: GO:0043467 regulation of generation of precursor metabolites and energy (IEA and ISO, transferred from human RBPJ) from KEEP_AS_NON_CORE to MARK_AS_OVER_ANNOTATED. The source is a single-gene COX4I2 activation result PMID:23303788, which the human review marks as over-annotated. The earlier mouse summary was a generic phenotype text that did not describe this term.
• Changed: GO:0061629 and GO:0140297 (IEA and ISO, transferred from human RBPJ) from ACCEPT to KEEP_AS_NON_CORE, matching human. The human sources are SPEN corepressor binding (MODIFIED there to corepressor binding) and minor co-binding reports. The term is independently true for mouse because Rbpj binds Ptf1a (PMID:11318877), but that is a tissue-specific function.
• Not changed, documented: human marks transfers of cross-pathway terms (BMP, ERBB and ephrin signalling) as over-annotated. Mouse holds the experimental IMP source (PMID:17336907) and keeps it non-core, consistent with its handling of other pleiotropic Rbpj IMP phenotypes. Worm lag-1 MODIFYs general transcription-regulation terms to GO:0007221; mouse ACCEPTs them as correct but general, and GO:0007221 is already accepted.
• Status set to COMPLETE.