Disease relevance of Cnbp

• Our results suggest that the Znf9 haploinsufficiency contributes to the myotonic dystrophy phenotype in Znf9(+/-) mice [1].
• Identification and characterization of a JC virus pentanucleotide repeat element binding protein: cellular nucleic acid binding protein [2].

High impact information on Cnbp

• In these regions, Myc expression was absent, indicating CNBP targets Myc in rostral head formation [3].
• The zinc-finger protein CNBP is required for forebrain formation in the mouse [3].
• In Cnbp(-/-) embryos, the visceral endoderm remains in the distal tip of the conceptus and the ADE fails to form, whereas the node and notochord form normally [3].
• A substantial reduction in cell proliferation was observed in the anterior regions of Cnbp(-/-) embryos at gastrulation and neural-fold stages [3].
• We show that the defects are caused by disruption of the gene encoding cellular nucleic acid binding protein (CNBP); Cnbp transgenic mice were able to rescue fully the mutant phenotype [3].

Biological context of Cnbp

• During mouse embryogenesis, CNBP is expressed in the anterior region of the early embryo and in the limb, tail and craniofacial region [4].
• Each of the mouse clones exhibited extraordinary sequence conservation with human CNBP cDNA, and the predicted mouse amino acid sequence identities with human CNBP protein ranged from 99 to 100% [5].
• Human cellular nucleic acid binding protein (CNBP) is a zinc finger DNA binding protein of unknown function [5].
• Genetic mapping of CNBP genes in interspecific and intersubspecific mouse backcrosses revealed two loci that hybridize to CNBP cDNA at high stringency, located on chromosomes 5 and 6 [5].
• These results offer novel insights into the function of CNBP during organogenesis as the regulator of forebrain formation and a number of rostral head transcription factors [6].

Anatomical context of Cnbp

• Znf9 is normally highly expressed in heart and skeletal muscle, where skeletal muscle chloride channel 1 (Clc1) plays an important role [1].
• Our findings demonstrate that Cnbp is essential for the forebrain induction and specification [3].
• CNBP was found in the cytosol and the endoplasmic reticulum in subcellular fractions from mouse liver, but was undetectable in nuclear fractions [5].
• Our data show that CNBP is expressed in tissues of early chick embryo that are the equivalent to the mouse embryo [6].
• Mutational analysis revealed that loss of CNBP binding leads to a decrease in CSF-1 promoter activity in fibroblasts but has no effect on CSF-1 promoter activity in monocytes [7].

Associations of Cnbp with chemical compounds

• CNBP is mainly conformed by seven retroviral Cys-Cys-His-Cys zinc-knuckles and a glycine/arginine rich region box [8].

Regulatory relationships of Cnbp

• Overexpression of CNBP strongly stimulates cell proliferation and increases c-myc promoter activity [4].

Other interactions of Cnbp

• Clc1 expression was dramatically decreased in Znf9(+/-) mice [1].
• Regulation of mouse colony-stimulating factor-1 gene promoter activity by AP1 and cellular nucleic acid-binding protein [7].
• These 4 genes were uncoupling protein 2, nucleolar spindle-associated protein, cellular nucleic acid-binding protein, and a novel acetyltransferase-like protein [9].

Analytical, diagnostic and therapeutic context of Cnbp

• Molecular cloning, developmental expression, promoter analysis and functional characterization of the mouse CNBP gene [4].
• Site-directed mutagenesis replacing the PKA phospho-acceptor amino acid residue impairs CNBP phosphorylation, suggesting that phosphorylation may not only exist in D. rerio but also in other vertebrates [8].

References