Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity

Annotation inferences using phylogenetic trees

Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt

Gene Ontology annotation based on curation of immunofluorescence data

Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara

Electronic Gene Ontology annotations created by ARBA machine learning models

Functional studies of BCL11A: characterization of the conserved BCL11A-XL splice variant and its interaction with BCL6 in nuclear paraspeckles of germinal center B cells.

BCL11A represses HBG transcription in K562 cells.

Proteomic and bioinformatic analysis of mammalian SWI/SNF complexes identifies extensive roles in human malignancy.

Direct Promoter Repression by BCL11A Controls the Fetal to Adult Hemoglobin Switch.

ALK mutants bind type I TKIs

Formation of neuronal progenitor BAF (npBAF)

SMARCA4, BCL11A,B-containing ATPase module binds SMARCC1:SMACC2 dimer:SMARCD1:SMARCE1:SMARCB1:ARID1A:DPF2, PHF10

Human EVI9, a homologue of the mouse myeloid leukemia gene, is expressed in the hematopoietic progenitors and down-regulated during myeloid differentiation of HL60 cells.

BCL11A is a SUMOylated protein and recruits SUMO-conjugation enzymes in its nuclear body.

Bcl11A/CTIP1 mediates the effect of the glutamate receptor on axon branching and dendrite outgrowth.

X-linked mental retardation gene CASK interacts with Bcl11A/CTIP1 and regulates axon branching and outgrowth.

BCL11A Haploinsufficiency Causes an Intellectual Disability Syndrome and Dysregulates Transcription.

Corrected and Republished from: BCL11A Is a Critical Component of a Transcriptional Network That Activates RAG Expression and V(D)J Recombination.

Structural insights into the DNA-binding mechanism of BCL11A: The integral role of ZnF6.

A tetramer of BCL11A is required for stable protein production and fetal hemoglobin silencing.