Immunization with recombinant ORF2 p551 protein protects common marmosets (Callithrix jacchus) against homologous and heterologous hepatitis E virus challenge.

Background: Hepatitis E virus (HEV) is a major causative agent of acute hepatitis worldwide, prompting continuous HEV vaccine efforts. Vaccine development is hampered by the lack of convenient animal models susceptible to infection with different HEV genotypes. We produced recombinant open reading frame 2 protein (pORF2; p551) of HEV genotype (GT) 3 and assessed its immunogenicity and protectivity against HEV challenge in common marmosets (Callithrix jacchus, CM).

Modulation of DNA binding properties of CCAAT/enhancer binding protein epsilon by heterodimer formation and interactions with NFkappaB pathway.

C/EBP epsilon is a transcription factor involved in myeloid cell differentiation. Along with C/EBP-alpha, -beta, -gamma, -delta, and -zeta, C/EBP-epsilon belongs to the family of CCAAT/enhancer binding proteins that are implicated in control of growth and differentiation of several cell lineages in inflammation and stress response. We have previously shown that C/EBP-epsilon preferentially binds DNA as a heterodimer with other C/EBP family members such as C/EBP-delta, CHOP (C/EBP-zeta), and the b-zip family protein ATF4.

KLF6: mutational analysis and effect on cancer cell proliferation.

Kruppel-like factor 6 (KLF6/Zf9/CPBP), a member of the Kruppel-like family of zinc finger transcription factors, has recently been suggested to be a mutated tumor suppressor in selected human cancers. Initially, we investigated whether the KLF6 gene was altered in 36 paired non-small cell lung cancers (NSCLC), 89 brain tumors, 7 normal brains, 46 cancer cell lines from a large variety of tissues, and 144 peripheral blood cells from healthy individuals using single strand conformation polymorphism (PCR-SSCP) and DNA sequencing. Changes in the coding region of KLF6 were found in brain tumors (missense changes, 8%; silent polymorphisms, 2%), lung cancers (missense changes, 3%; silent polymorphisms, 6%) and cancer cell lines (missense changes, 2%; silent polymorphisms, 2%).

CCAAT/enhancer binding protein epsilon: changes in function upon phosphorylation by p38 MAP kinase.

C/EBPepsilon, a member of the CCAAT/enhancer binding protein family, is a transcription factor important in neutrophil differentiation. We have determined that it is phosphorylated on multiple serine and threonine residues and can be a target for phosphorylation by a number of kinases. We identified a threonine at amino acid 75, part of a consensus mitogen-activated protein (MAP) kinase site within the transactivation domain of C/EBPepsilon, as being phosphorylated only by p38 MAP kinase.

Protein partners of C/EBPepsilon.

CCAAT-enhancer binding protein-epsilon (C/EBPepsilon) is a nuclear transcription factor implicated in the regulation of terminal myeloid differentiation. Using a yeast two-hybrid screen, potential interaction partners of C/EBPepsilon involved in myeloid development were identified. C/EBPepsilon was found to associate with other C/EBP family members, including C/EBPepsilon and CHOP as well as other proteins that are known to contain a leucine-zipper protein interaction motif including CREB2, LDOC1, E6TP1, and AF-17.

Identification of murine and human XCP1 genes as C/EBP-epsilon-dependent members of FIZZ/Resistin gene family.

The CCAAT enhancer binding protein epsilon (C/EBP-epsilon) transcription factor is expressed predominantly in granulocytes. Mice with a disruption of the C/EBP-epsilon gene fail to produce mature granulocytes and eosinophils. Cells derived from the peritoneal exudates of C/EBP-epsilon -/- mice lack the expression of a number of chemokines and chemokine receptor genes.