Disease relevance of ZBTB7B

• Maximal increase in promoter activity in hypoxia was observed between -190 and -174 bp of the proximal promoter, once a cKrox repressor site (-199 to -224 bp) was deleted [1].

High impact information on ZBTB7B

• The c-Krox protein contains three zinc fingers of the Cys2His2 type. c-Krox binds specifically to a guanine-rich cis-acting element present twice in the promoter element of the mouse alpha 1(I) collagen gene [2].
• DNA transfection experiments in mouse NIH 3T3 fibroblasts, cells that express the c-Krox gene, or in Drosophila S2 cells, which do not express c-Krox, reveal that c-Krox can activate transcription of a reporter gene linked to several copies of its binding site in the alpha 1(I) collagen promoter [2].
• c-Krox, a transcriptional regulator of type I collagen gene expression, is preferentially expressed in skin [2].
• The selective spatial pattern of expression of its mRNA and its transcription activation ability suggest that c-Krox may be an important regulator of type I collagen skin specific expression in physiologic conditions and in fibrotic diseases such as scleroderma [2].
• In addition, OCZF specifically bound to the guanine-rich consensus sequences of Egr-1 and c-Krox [3].

Biological context of ZBTB7B

• This region was extensively analyzed by DNAse footprinting and electrophoretic mobility shift assays, and a putative binding site for the transcription factor c-Krox was discovered [4].
• Both contain three kruppel-like zinc-finger DNA binding motifs that are 71-78% identical to those of hcKrox-alpha [5].
• Cloning and characterization of hcKrox, a transcriptional regulator of extracellular matrix gene expression [6].
• Transient transfection assays indicate that hcKrox represses transcription of the alpha1(I) procollagen promoter, and electrophoretic mobility shift assays demonstrate that hcKrox binds to both the human and murine promoter DNA [6].
• In the mouse, cKrox is expressed, beginning at 9.5 days of gestation and at 10.5 days in regions destined to become skin [6].

Anatomical context of ZBTB7B

• The expression of c-Krox in bone was then examined by reverse-transcribed polymerase chain reaction and Northern blotting analysis; an approximately 3.4 kb transcript was detected in primary osteoblastic cells, in MG-63 cells, and in human bone marrow stromal cells [4].
• RT-PCR analysis of human fibroblasts indicates constitutive low-level expression of cKrox which can be transiently elevated by treatment with retinoic acid [6].
• Demethylation of CpG sequences in lymphocytes, in which CpG sequences were heavily methylated, induced CDCP1 expression and its expression level further increased through zfp67 overexpression [7].

Physical interactions of ZBTB7B

• Amount of zfp67 in Jurkat was comparable with K562, but chromatin immunoprecipitation showed that zfp67 bound to CDCP1 promoter in K562 but not in Jurkat [7].

Other interactions of ZBTB7B

• The reporter assay and si-RNA-mediated knockdown experiment revealed that zfp67, a zinc-finger protein, enhanced CDCP1 transcription [7].

Analytical, diagnostic and therapeutic context of ZBTB7B

• RT-PCR experiments demonstrate that all three hcKrox family members are expressed in foreskin and dermal fibroblasts [5].
• Immunoprecipitation studies indicate that cKrox can form heterodimers in solution in the absence of DNA [5].

References