Transcription regulator that acts as a key regulator of lineage commitment of immature T-cell precursors. Exerts distinct biological functions in the mammary epithelial cells and T cells in a tissue-specific manner (PubMed:15729333, PubMed:29420538). Necessary and sufficient for commitment of CD4 lineage, while its absence causes CD8 commitment. Development of immature T-cell precursors (thymocytes) to either the CD4 helper or CD8 killer T-cell lineages correlates precisely with their T-cell receptor specificity for major histocompatibility complex class II or class I molecules, respectively. Cross-antagonism between ZBTB7B and CBF complexes are determinative to CD4 versus CD8 cell fate decision (PubMed:15729333, PubMed:24880459, PubMed:18258917, PubMed:23481257). Suppresses RUNX3 expression and imposes CD4+ lineage fate by inducing the SOCS suppressors of cytokine signaling. induces, as a transcriptional activator, SOCS genes expression which represses RUNX3 expression and promotes the CD4+ lineage fate (PubMed:24880459). During CD4 lineage commitment, associates with multiple sites at the CD8 locus, acting as a negative regulator of the CD8 promoter and enhancers by epigenetic silencing through the recruitment of class II histone deacetylases, such as HDAC4 and HDAC5, to these loci (PubMed:22730529). Regulates the development of IL17-producing CD1d-restricted naural killer (NK) T cells (PubMed:23105140). Also functions as an important metabolic regulator in the lactating mammary glands. Critical feed-forward regulator of insulin signaling in mammary gland lactation, directly regulates expression of insulin receptor substrate-1 (IRS-1) and insulin-induced Akt-mTOR-SREBP signaling (PubMed:29420538). Transcriptional repressor of the collagen COL1A1 and COL1A2 genes. May also function as a repressor of fibronectin and possibly other extracellular matrix genes (PubMed:7937772). Potent driver of brown fat development, thermogenesis and cold-induced beige fat formation (PubMed:28784777). Recruits the brown fat lncRNA 1 (Blnc1):HNRNPU ribonucleoprotein complex to activate thermogenic gene expression in brown and beige adipocytes (PubMed:28784777). Homodimerizes (PubMed:22730529). Interacts with NCL, NEDD4 and YBX1 (PubMed:28784777). Interacts with HNRNPU (via RNA-binding RGG-box region); the interaction facilitates the recruitment of long non-coding RNA Blnc1 by ZBTB7B (PubMed:28784777). Interacts with HDAC4 and HDAC5; the interaction allows the recruitment of HDAC4 and HDAC5 on CD8 loci for deacetylation and possible inhibition of CD8 genes expression (PubMed:22730529). Widely expressed, with a higher level in skin. Expressed in thymus. Restricted to CD4 cells (mature single positive CD4(+) and intermediate CD4(+)CD8(+) cells). Expressed in the luminal epithelial cells in the mammary glands where is up-regulated at late pregnancy and lactation (PubMed:29420538). Expression is enriched in brown fat (PubMed:28784777). Expressed, beginning at 9.5 days of gestation and at 10.5 days in regions destined to become skin. In adult animals, expression is predominantly in skin (PubMed:7937772). Expression is significantly increased during brown adipocyte differentiation (PubMed:28784777). Expression in mammary glands is induced by insulin. Acetylated directly and specifically by EP300. EP300-mediated acetylation of Lys-210, Lys-216 and Lys-339 stabilizes the protein by antagonizing ubiquitin conjugation. Ubiquitinated, leading to proteasomal degradation. Competes with acetylation on Lys-210, Lys-216 and Lys-339. Defects in Zbtb7b are the cause of helper deficient disease (HD) or helpless disease. HD and helpless mice are distinguished by the virtual absence of peripheral T-cells of the CD4(+)CD8(-) major histocompatibility complex (MHC) class II-restricted T-helper subset due to a specific block in thymic development. The developmental defect is selective for CD4(+)CD8(-) cells; the maturation of CD4(-)CD8(+) and gamma delta T-cells is normal indicating that lineage commitment is specifically perturbed without affecting positive selection. In helpless disease, NKT cells are hyperproliferative, most lack CD4 and instead express CD8. The majority of NKT cells in the thymus produce IL17 with high frequency while very few produce IFNG or other cytokines (PubMed:23105140). Mutant females are unable to efficiently secrete milk lipid and to nurse the offspring. They show normal mammary gland morphogenesis in puberty and alveologenesis in pregnancy, but are defective in triggering the onset of lactation upon parturition with large cellular lipid droplets retained within alveolar epithelial cells (PubMed:29420538). Mice are more sensitive to cold temperature, with impaired cold-induced transcriptional remodeling in brown fat and diminished browning of inguinal white fat (PubMed:28784777). Chimeric cDNA. Chimeric cDNA.