Gene Ontology annotation through association of InterPro records with GO terms

Annotation inferences using phylogenetic trees

Combined Automated Annotation using Multiple IEA Methods

LAF-4 encodes a lymphoid nuclear protein with transactivation potential that is homologous to AF-4, the gene fused to MLL in t(4;11) leukemias.

A mutation in Af4 is predicted to cause cerebellar ataxia and cataracts in the robotic mouse.

The synthetic peptide PFWT disrupts AF4-AF9 protein complexes and induces apoptosis in t(4;11) leukemia cells.

The mixed-lineage leukemia fusion partner AF4 stimulates RNA polymerase II transcriptional elongation and mediates coordinated chromatin remodeling.

AF4 is a critical regulator of the IGF-1 signaling pathway during Purkinje cell development.

AFF4, a component of the ELL/P-TEFb elongation complex and a shared subunit of MLL chimeras, can link transcription elongation to leukemia.

Human mediator subunit MED26 functions as a docking site for transcription elongation factors.

Global landscape of HIV-human protein complexes.

The little elongation complex regulates small nuclear RNA transcription.

The super elongation complex family of RNA polymerase II elongation factors: gene target specificity and transcriptional output.

Leukemia fusion target AF9 is an intrinsically disordered transcriptional regulator that recruits multiple partners via coupled folding and binding.

AFF1 is a ubiquitous P-TEFb partner to enable Tat extraction of P-TEFb from 7SK snRNP and formation of SECs for HIV transactivation.

AFF1 and AFF4 differentially regulate the osteogenic differentiation of human MSCs.

AFF1 acetylation by p300 temporally inhibits transcription during genotoxic stress response.

Stabilization of AFF1 by PARylation ensures transcriptional restart after DNA damage.

UniProt entry P51825 (AFF1_HUMAN)

AFF1 (P51825) annotation-provenance analysis

Affinage mechanistic annotation for AFF1 (human)