Protein AF1q (AF1q)

Protein AF1q (MLLT11), also known as ALL1-fused gene from chromosome 1q, is a 90-amino-acid protein initially discovered as a fusion partner in translocations causing acute myeloid leukemia. AF1q functions as a transcriptional cofactor, notably enhancing Wnt/β-catenin and STAT3 signaling through physical interactions with transcription factors such as TCF7. AF1q drives hematopoietic lineage differentiation toward the T-cell fate via cooperation with Notch signaling, restricts B-cell development, and influences cell cycle and apoptosis. Pathologically, AF1q is consistently overexpressed in several cancers, conferring poor prognosis, promoting migration, invasion, and tumorigenicity—especially in neuroblastoma, breast, and lung cancers. There are no direct therapeutics against AF1q currently, but it functions as a promising biomarker and potential therapeutic target, with inhibition of its downstream effector pathways under investigation.

Other names

MLLT11ALL1-fused gene from chromosome 1qAF1QMLLT11 transcription factor 7 cofactormyeloid/lymphoid or mixed-lineage leukemia (trithorax homolog, Drosophila); translocated to, 11

Drugs targeting AF1q-driven malignancies could act by: Inhibiting associated signaling cascades (e.g., PDGF-B/PDGFR or STAT3, Wnt/TCF7); Promoting AF1q degradation (e.g., proteasomal activation)