BIK
BCL2 interacting killer | NBK

The protein encoded by this gene shares a critical BH3 domain with other death-promoting proteins, such as BID, BAK, BAD and BAX, that is required for its pro-apoptotic activity, and for interaction with anti-apoptotic members of the BCL2 family, and viral survival-promoting proteins. Since the activity of this protein is suppressed in the presence of survival-promoting proteins, it is suggested as a likely target for anti-apoptotic proteins. [provided by RefSeq, Sep 2011]

Biological processes 11 terms
Expression (TPM)
BIK — as a Regulated Gene

TFs regulating BIK 0 TFs

Transcription factors with Perturb-seq knockdown data for BIK. The Binding column indicates whether any binding evidence exists for this TF–gene pair (ChIP-seq or motif footprint peaks). The Mean coef is the average Perturb-seq regression coefficient across active gRNAs (positive = BIK upregulated upon KD; negative = downregulated). The Outlier column indicates whether this gene is in the top or bottom 5% of all TF knockdown effects.

Data: Effect:
TF Mean coef Binding Outlier TF→Gene link

Elements linked to BIK

Open chromatin peaks (ATAC-seq) in the genomic neighbourhood of BIK, linked by TSS proximity or chromatin conformation (Multiome / HiCAR). Each element overlaps at least one TF ChIP-seq binding site — the TFs column shows how many distinct TFs bind that element.

Accessibility Element Dist. to TSS Link type TFs
chr22:43,110,485–43,111,495 at TSS At TSS 485

Genome Browser

Genomic view of the BIK locus showing ATAC-seq accessibility and RNA-seq expression across the ESC → DE time course, together with TF binding peaks and element-to-TSS loop connections.

chr22:43,100,485 – 43,121,495
Proximal 1 kb Distal 10 kb Multiome HiCAR ATAC-seq RNA-seq