Stefan Schwartz
Professor vid Institutionen för medicinsk biokemi och mikrobiologi; Infektioner och immunitet; Stefan Schwartz
- Mobiltelefon:
- 073-980 62 33
- E-post:
- stefan.schwartz@imbim.uu.se
- Besöksadress:
- BMC
Husargatan 3
752 37 UPPSALA - Postadress:
- Box 582
751 23 UPPSALA
- Akademiska meriter:
- DMSc
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Publikationer
Senaste publikationer
- RNA elements that control human papillomavirus mRNA splicing-targets for therapy? (2024)
- HnRNP D activates production of HPV16 E1 and E6 mRNAs by promoting intron retention (2022)
- Overexpression of m6A-factors METTL3, ALKBH5, and YTHDC1 alters HPV16 mRNA splicing. (2022)
- Identification of heterogenous nuclear ribonucleoproteins (hnRNPs) and serine- and arginine-rich (SR) proteins that induce human papillomavirus type 16 late gene expression and alter L1 mRNA splicing (2022)
- hnRNP G/RBMX enhances HPV16 E2 mRNA splicing through a novel splicing enhancer and inhibits production of spliced E7 oncogene mRNAs (2022)
Alla publikationer
Artiklar
- RNA elements that control human papillomavirus mRNA splicing-targets for therapy? (2024)
- HnRNP D activates production of HPV16 E1 and E6 mRNAs by promoting intron retention (2022)
- Overexpression of m6A-factors METTL3, ALKBH5, and YTHDC1 alters HPV16 mRNA splicing. (2022)
- Identification of heterogenous nuclear ribonucleoproteins (hnRNPs) and serine- and arginine-rich (SR) proteins that induce human papillomavirus type 16 late gene expression and alter L1 mRNA splicing (2022)
- hnRNP G/RBMX enhances HPV16 E2 mRNA splicing through a novel splicing enhancer and inhibits production of spliced E7 oncogene mRNAs (2022)
- The role of RNA-binding proteins in the processing of mRNAs produced by carcinogenic papillomaviruses (2022)
- Inefficient splicing of segment 7 and 8 mRNAs is an inherent property of influenza virus A/Brevig Mission/1918/1 (H1N1) that causes elevated expression of NS1 protein (2012)
- Serine/arginine-rich protein 30c activates human papillomavirus type 16 L1 mRNA expression via a bimodal mechanism (2011)
- Inhibition of splicing by serine-arginine rich protein 55 (SRp55) causes the appearance of partially spliced HIV-1 mRNAs in the cytoplasm (2011)
- Multiple ASF/SF2 Sites in the Human Papillomavirus Type 16 (HPV-16) E4-Coding Region Promote Splicing to the Most Commonly Used 3'-Splice Site on the HPV-16 Genome (2010)
- Serine- and Arginine-rich Proteins 55 and 75 (SRp55 and SRp75) Induce Production of HIV-1 vpr mRNA by Inhibiting the 5 '-Splice Site of Exon 3 (2010)
- Increased expression of cellular RNA-binding proteins in HPV-induced neoplasia and cervical cancer (2009)
- Adenovirus E4orf4 induces HPV-16 late L1 mRNA production (2009)
- HPV-16 RNA processing (2008)
- Polypyrimidine tract binding protein induces human papillomavirus type 16 late gene expression by interfering with splicing inhibitory elements at the major late 5' splice site, SD3632 (2008)
- Inhibition of HPV-16 L1 expression from L1 cDNAs correlates with the presence of hnRNP A1 binding sites in the L1 coding region (2008)
- Identification of a 17-nucleotide splicing enhancer in HPV-16 L1 that counteracts the effect of multiple hnRNP A1-binding splicing silencers (2007)
- The presence of inhibitory RNA elements in the late 3'-untranslated region is a conserved property of human papillomaviruses (2007)
- A splicing enhancer in the E4 coding region of human papillomavirus type 16 is required for early mRNA splicing and polyadenylation as well as inhibition of premature late gene expression. (2005)
- A 57-nucleotide upstream early polyadenylation element in human papillomavirus type 16 interacts with hFip1, CstF-64, hnRNP C1/C2, and polypyrimidine tract binding protein (2005)
- A Downstream Polyadenylation Element in Human Papillomavirus Type 16 L2 Encodes Multiple GGG Motifs and Interacts with hnRNP H (2005)
- HPV-16 L1 genes with inactivated negative RNA elements induce potent immune responses. (2004)
- Identification of an hnRNP A1-dependent splicing silencer in the human papillomavirus type 16 L1 coding region that prevents premature expression of the late L1 gene. (2004)
