Tanel Punga

Functional inactivation of the SR family of splicing factors during a vaccinia virus infection.

Adenovirus 2 E1B-55K protein relieves p53-mediated transcriptional repression of the survivin and MAP4 promoters.

YY1 inhibits the activation of the p53 tumor suppressor in response to genotoxic stress.

Hyperphosphorylation regulates the activity of SREBP1 during mitosis.

Phosphorylation and ubiquitination of the transcription factor sterol regulatory element-binding protein-1 in response to DNA binding.

Novel genes in cell cycle control and lipid metabolism with dynamically regulated binding sites for sterol regulatory element-binding protein 1 and RNA polymerase II in HepG2 cells detected by chromatin immunoprecipitation with microarray detection.

Long intronic GAA repeats causing Friedreich ataxia impede transcription elongation.

Dicer associates with chromatin to repress genome activity in Schizosaccharomyces pombe.

Two cellular protein kinases, DNA-PK and PKA, phosphorylate the adenoviral L4-33K protein and have opposite effects on L1 alternative RNA splicing.

The adenovirus VA RNA-derived miRNAs are not essential for lytic virus growth in tissue culture cells.

Muscle-specific regulation of the mTOR signaling pathway in MuSK antibody seropositive (MuSK+) experimental autoimmune Myasthenia gravis (EAMG).

Adenovirus precursor pVII protein stability is regulated by its propeptide sequence.

Small RNA sequence analysis of adenovirus VA RNA-derived miRNAs reveals an unexpected serotype-specific difference in structure and abundance.

Circulating miRNAs in myasthenia gravis: miR-150-5p as a new potential biomarker.

A splice variant of the human phosphohistidine phosphatase 1 (PHPT1) is degraded by the proteasome.

Genome-Engineering Tools to Establish Accurate Reporter Cell Lines That Enable Identification of Therapeutic Strategies to Treat Friedreich's Ataxia.

Opposite expression of CYP51A1 and its natural antisense transcript AluCYP51A1 in adenovirus type 37 infected retinal pigmented epithelial cells.

Disease specific signature of circulating miR-150-5p and miR-21-5p in myasthenia gravis patients.

Complementation of the human adenovirus type 5 VA RNAI defect by the Vaccinia virus E3L protein and serotype-specific VA RNAIs.

A suppressive effect of Sp1 recruitment to the first leader 5' splice site region on L4-22K-mediated activation of the adenovirus major late promoter.