GFI1B recognizes regulatory DNA and recruits transcriptional corepressors. The evidence below separates human natural products, engineered reagents and murine experiments; it does not assign every perturbation phenotype a direct molecular role.
PMID:22399799(https://pubmed.ncbi.nlm.nih.gov/22399799/) distinguishes human p32 and p37 in erythroid systems. The short-product depletion and comparative recruitment experiments support hematopoietic repression. The p37 overexpression condition also increases endogenous p32. Synthetic methylated peptides and K8A mutants test recruitment requirements; they do not quantify endogenous Lys8 modification. The observed p39 band has no identified transcript.
PMID:9566867(https://pubmed.ncbi.nlm.nih.gov/9566867/) uses murine cDNA and mouse cells. Its p21 repression and inhibition of IL6-induced arrest have the opposite sign from the incoming negative-G1/S assertion. PMID:12351384(https://pubmed.ncbi.nlm.nih.gov/12351384/) also uses murine cDNA, including in human recipient cells. Its artificial consensus-site reporter and SOCS1 promoter have different responses; activation cannot be generalized across promoters.
The original PMID:15920471 article, Results accompanying Figure 1D, states: “FOG‐1 antibodies immunoprecipitated GATA‐1 but not TAL‐1, Ldb1 or Gfi‐1b”. This is a reported mouse MEL assay, not a universal no-interaction claim. Its positive GATA1/Gfi1b complex is distinct. The literal incoming Q8IX07 accession identifies FOG1/ZFPM1 and remains unchanged pending a source-context check. The local publication cache contains the abstract; this statement comes from the independently accessed original.
The original supplemental workbook for PMID:28473536 supplies the following derived target index, using one-based Excel row numbers:
| Target | Protein row | Displayed-sequence coordinates | Motif model rows |
|---|---|---|---|
| GFI1B | S1:785 | residues 148–330 | S2:7543/7548 |
The 183-residue extended DNA-binding reagent exactly matches positions 148–330 of the 330-residue product. It is neither the full-length p37 protein nor p32. S2 contains methylated and unmethylated selection models; no GFI1B-specific S3 classification or native promoter occupancy is inferred. Methods describe recombinant bacterial protein selection on random DNA. The more specific regulatory-DNA judgment also uses independent promoter evidence and the actual ancestral assertion.
PMID:16713569(https://barabasi.com/media/pub_imports/files/190.pdf) reports the inherited-ataxia interaction screen. Six exact positive IntAct records preserve the NELL2, CPAP/CENPJ and JAG2 pairs in Y2H and HEK293T pull-down assays. CPAP records EBI-952822 and EBI-946647 supply pair-specific evidence; the study-wide validation rate does not. The 1–330 target feature is not a clone-sequence or isoform crosswalk. CPAP FUNCTION establishes its microtubule-regulatory class, matching GO:0005519. The signaling terms GO:0038023 and GO:0048018 instead require signal transmission or a change in receptor activity; binding NELL2 or putative ligand JAG2 demonstrates neither. None of these assays establishes endogenous colocalization or a cytoskeletal role for GFI1B.
The asserted PAINT book is PTHR24393, while the current UniProt cross-reference is PTHR23226:SF419. Both are retained as different source assertions. The actual 330-residue target AN43/PTN002550783 descends from the four-function AN0/PTN002811836 node and the hematopoiesis AN29/PTN008616677 node. Donor count and target self-evidence do not weaken those assertions. No replacement family assignment is made.
PMID:16177182(https://pubmed.ncbi.nlm.nih.gov/16177182/), Methods “Plasmid constructs and site-directed mutagenesis” and Results accompanying Figures 6 and 8, tests human GFI1B with tagged mouse GATA1 in 293T cells and GATA1-dependent recruitment in human K562 cells. The positive cellular association supports transcription-factor binding independently of the retained FOG1 source query. Discussion also reports no interaction in the tested yeast two-hybrid system; purified direct affinity is not established.
The human p32 experiments in PMID:22399799 support erythroid regulation. PMID:23927492(https://pubmed.ncbi.nlm.nih.gov/23927492/) and PMID:24325358(https://pubmed.ncbi.nlm.nih.gov/24325358/) describe altered transcriptional activity and abnormal megakaryocyte development or marker expression in human GFI1B disease contexts; only their abstracts were inspected. These observations refine the conserved hemopoiesis assertion to two regulatory lineages, without creating a new ancestral node or assigning both products identical roles.