Burghardt Wittig

Last updated

Burghardt Wittig (born 1947 in Celle, Germany) is the chairman of MolBio2Math and a professor of biochemistry and molecular biology at Freie Universitaet Berlin in Berlin (FUB), Germany. [1] His research focuses on the areas of gene regulation, DNA structures induced by torsional strain, chromatin structure, G-protein-mediated signal transduction, as well as therapeutic applications of genetic research and DNA-based vaccines. His research has been published in numerous leading scientific journals, including Cell, Nature, PNAS, and Science.

Contents

Early life

Wittig was born in Celle, Germany, where he attended the classical "Gymnasium Ernestinum". He graduated by the German Abitur in fall 1966, followed by two years of service in the German military. [1]

Career and Research

Wittig enrolled at Freie Universitaet Berlin in 1968 to study medicine. While attending medical school, he also received training as an engineer specialised in hearing aids (audiologist) and graduated by the German Gesellenpruefung. During his time as a medical student at Freie Universitaet Berlin, Wittig joined laboratories at the Institute of Molecular Biology and Biochemistry and at the Max Planck Institute for Molecular Genetics to conduct the experiments for his MD thesis. He was principally mentored by Hubert Gottschling but received further advice from V.A. Erdmann, O. Pongs, H.-J. Risse, H. Tiedemann and H.G. Wittmann as well. Having concluded his medical studies in 1975, Wittig successfully defended his thesis on "Purification and Characterisation of the Four Lysine-Specific Transfer Ribonucleic Acids from Chicken Embryos" (German: Reinigung und Charakterisierung der vier lysinspezifischen Transfer-Ribonukleinsäuren aus Hühnerembyronen) in 1976. He stayed at Freie Universitaet as a postdoc until 1978, and as an assistant professor from 1978 to 1987. [1]

From 1976 to 1986, Wittig attended a variety of physics courses in addition to his principal work as a researcher. These classes led him as a visiting student to Technische Universitaet Berlin, California Institute of Technology (Caltech) and Massachusetts Institute of Technology (MIT). He received no official degree for these courses. [1]

In 1980, Wittig habilitated for "Biochemistry and Molecular Biology" and became thus formally eligible for a full professorship in Germany. For the 1982/83 cycle, Wittig was awarded a Heisenberg scholarship of the Deutsche Forschungsgemeinschaft; he continued to work as a fellow of the programme until 1989. During this time, he spent time at the labs of Edward Trifonov at the Weizmann Institute of Science, Rehovot, and Koki Horikoshi, at Riken. [1]

From 1984 to 1986, Wittig worked as a visiting professor at Alexander Rich's lab at MIT, where he also cooperated with Alexander Varshavsky. Wittig would later describe these years as "the most career-shaping of [his] life". [2]

In 1987, Freie Universitaet Berlin awarded Wittig an extraordinary professorship. He continued to work as a visiting professor at Alexander Rich's lab until 1989, when he became a Schering professor (S-C4, full tenure) at Freie Universitaet Berlin. In 1988, he became the fully tenured founding chair and department head of Molecular Biology and Bioinformatics at Freie Universitaet's Institute of Molecular Biology and Biochemistry. After a change of the relevant laws of the state of Berlin merged parts of Freie Universitaet and Humboldt Universitaet into the Charité – Universitaetsmedizin, Wittig became director of its newly founded Institute of Molecular Biology and Bioinformatics. [1]

Beginning in 1994, Wittig focused his research on the design, development, and clinical proof-of-concept of covalently closed DNA constructs for the treatment of cancer and for DNA-vaccines against infectious diseases. [1] Two classes of DNA-molecules evolved through theoretical and experimental selection processes and became key technologies; MIDGE (minimalistic, immunogenically defined gene expression), and dSLIM for DNA-based immunomodulation. [3]

Guided by the goal of facilitating the independent transition from basic research into clinical DNA-based medicines, Wittig founded Mologen AG in 1998. The firm had their IPO at the German stock exchange in the same year. [4] He served as Mologen AG's CEO until 2007, while continuing to work as a full professor in a private-public-partnership.

In 2010, Wittig's institute returned to Freie Universitaet Berlin as a non-profit foundation with Freie Universitaet as the trustee. He served as the chairman of this newly created Foundation Institute of Molecular Biology and Bioinformatics until 2017.

In late 2019, Wittig founded MolBio2Math, a non-profit foundation under the trusteeship of the Gentechnologiestiftung - Dr. Georg und Ingeburg Scheel Stiftung, of which he is currently the chairman [5]

Selected publications

Related Research Articles

p53 Mammalian protein found in Homo sapiens

p53, also known as Tumor protein P53, cellular tumor antigen p53, or transformation-related protein 53 (TRP53) is a regulatory protein that is often mutated in human cancers. The p53 proteins are crucial in vertebrates, where they prevent cancer formation. As such, p53 has been described as "the guardian of the genome" because of its role in conserving stability by preventing genome mutation. Hence TP53 is classified as a tumor suppressor gene.

Antigenic drift is a kind of genetic variation in viruses, arising from the accumulation of mutations in the virus genes that code for virus-surface proteins that host antibodies recognize. This results in a new strain of virus particles that is not effectively inhibited by the antibodies that prevented infection by previous strains. This makes it easier for the changed virus to spread throughout a partially immune population. Antigenic drift occurs in both influenza A and influenza B viruses.

<span class="mw-page-title-main">Toll-like receptor</span> Pain receptors and inflammation

Toll-like receptors (TLRs) are a class of proteins that play a key role in the innate immune system. They are single-spanning receptors usually expressed on sentinel cells such as macrophages and dendritic cells, that recognize structurally conserved molecules derived from microbes. Once these microbes have reached physical barriers such as the skin or intestinal tract mucosa, they are recognized by TLRs, which activate immune cell responses. The TLRs include TLR1, TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, TLR10, TLR11, TLR12, and TLR13. Humans lack genes for TLR11, TLR12 and TLR13 and mice lack a functional gene for TLR10. The receptors TLR1, TLR2, TLR4, TLR5, TLR6, and TLR10 are located on the cell membrane, whereas TLR3, TLR7, TLR8, and TLR9 are located in intracellular vesicles.

<span class="mw-page-title-main">Peroxisome proliferator-activated receptor</span> Group of nuclear receptor proteins

In the field of molecular biology, the peroxisome proliferator-activated receptors (PPARs) are a group of nuclear receptor proteins that function as transcription factors regulating the expression of genes. PPARs play essential roles in the regulation of cellular differentiation, development, and metabolism, and tumorigenesis of higher organisms.

<span class="mw-page-title-main">Origin of replication</span> Sequence in a genome

The origin of replication is a particular sequence in a genome at which replication is initiated. Propagation of the genetic material between generations requires timely and accurate duplication of DNA by semiconservative replication prior to cell division to ensure each daughter cell receives the full complement of chromosomes. This can either involve the replication of DNA in living organisms such as prokaryotes and eukaryotes, or that of DNA or RNA in viruses, such as double-stranded RNA viruses. Synthesis of daughter strands starts at discrete sites, termed replication origins, and proceeds in a bidirectional manner until all genomic DNA is replicated. Despite the fundamental nature of these events, organisms have evolved surprisingly divergent strategies that control replication onset. Although the specific replication origin organization structure and recognition varies from species to species, some common characteristics are shared.

SV40 is an abbreviation for simian vacuolating virus 40 or simian virus 40, a polyomavirus that is found in both monkeys and humans. Like other polyomaviruses, SV40 is a DNA virus that sometimes causes tumors in animals, but most often persists as a latent infection. SV40 has been widely studied as a model eukaryotic virus, leading to many early discoveries in eukaryotic DNA replication and transcription.

Extrachromosomal DNA is any DNA that is found off the chromosomes, either inside or outside the nucleus of a cell. Most DNA in an individual genome is found in chromosomes contained in the nucleus. Multiple forms of extrachromosomal DNA exist, and, while some of these serve important biological functions, they can also play a role in diseases such as cancer.

<span class="mw-page-title-main">Viral vector</span> Biotechnology to deliver genetic material into a cell

Viral vectors are tools commonly used by molecular biologists to deliver genetic material into cells. This process can be performed inside a living organism or in cell culture. Viruses have evolved specialized molecular mechanisms to efficiently transport their genomes inside the cells they infect. Delivery of genes or other genetic material by a vector is termed transduction and the infected cells are described as transduced. Molecular biologists first harnessed this machinery in the 1970s. Paul Berg used a modified SV40 virus containing DNA from the bacteriophage λ to infect monkey kidney cells maintained in culture.

<span class="mw-page-title-main">Liver X receptor</span> Nuclear receptor

The liver X receptor (LXR) is a member of the nuclear receptor family of transcription factors and is closely related to nuclear receptors such as the PPARs, FXR and RXR. Liver X receptors (LXRs) are important regulators of cholesterol, fatty acid, and glucose homeostasis. LXRs were earlier classified as orphan nuclear receptors, however, upon discovery of endogenous oxysterols as ligands they were subsequently deorphanized.

<span class="mw-page-title-main">Gene delivery</span> Introduction of foreign genetic material into host cells

Gene delivery is the process of introducing foreign genetic material, such as DNA or RNA, into host cells. Gene delivery must reach the genome of the host cell to induce gene expression. Successful gene delivery requires the foreign gene delivery to remain stable within the host cell and can either integrate into the genome or replicate independently of it. This requires foreign DNA to be synthesized as part of a vector, which is designed to enter the desired host cell and deliver the transgene to that cell's genome. Vectors utilized as the method for gene delivery can be divided into two categories, recombinant viruses and synthetic vectors.

Demethylases are enzymes that remove methyl (CH3) groups from nucleic acids, proteins (particularly histones), and other molecules. Demethylases are important epigenetic proteins, as they are responsible for transcriptional regulation of the genome by controlling the methylation of DNA and histones, and by extension, the chromatin state at specific gene loci.

<span class="mw-page-title-main">Histidine ammonia-lyase</span>

Histidine ammonia-lyase is an enzyme that in humans is encoded by the HAL gene. It converts histidine into ammonia and urocanic acid. Its systematic name is L-histidine ammonia-lyase (urocanate-forming).

<span class="mw-page-title-main">RELA</span> Protein-coding gene in the species Homo sapiens

Transcription factor p65 also known as nuclear factor NF-kappa-B p65 subunit is a protein that in humans is encoded by the RELA gene.

<span class="mw-page-title-main">Peroxisome proliferator-activated receptor delta</span> Nuclear receptor protein found in humans

Peroxisome proliferator-activated receptor delta(PPAR-delta), or (PPAR-beta), also known as Nuclear hormone receptor 1(NUC1) is a nuclear receptor that in humans is encoded by the PPARD gene.

<span class="mw-page-title-main">MAFG</span> Protein-coding gene in the species Homo sapiens

Transcription factor MafG is a bZip Maf transcription factor protein that in humans is encoded by the MAFG gene.

<span class="mw-page-title-main">BRCC3</span> Protein-coding gene in humans

Lys-63-specific deubiquitinase BRCC36 is an enzyme that in humans is encoded by the BRCC3 gene.

DNA detailed study

Gary J. Nabel is an American virologist and immunologist who is President and chief executive officer of ModeX Therapeutics in Natick, Massachusetts.

RNA therapeutics are a new class of medications based on ribonucleic acid (RNA). Research has been working on clinical use since the 1990s, with significant success in cancer therapy in the early 2010s. In 2020 and 2021, mRNA vaccines have been developed globally for use in combating the coronavirus disease. The Pfizer–BioNTech COVID-19 vaccine was the first mRNA vaccine approved by a medicines regulator, followed by the Moderna COVID-19 vaccine, and others.

A nucleoside-modified messenger RNA (modRNA) is a synthetic messenger RNA (mRNA) in which some nucleosides are replaced by other naturally modified nucleosides or by synthetic nucleoside analogues. modRNA is used to induce the production of a desired protein in certain cells. An important application is the development of mRNA vaccines, of which the first authorized were COVID-19 vaccines.

References

  1. 1 2 3 4 5 6 7 "Burghardt Wittig". www.fu-berlin.de. 2012-06-04. Retrieved 2018-07-09.
  2. Zhang, Shuguang; Wittig, Burghardt (2015). "Alexander Rich 1924–2015". Nature Biotechnology. 33 (6): 593–598. doi:10.1038/nbt.3262. ISSN   1087-0156. PMID   26057974. S2CID   562909.
  3. "dSLIMming the immune system". BioCentury. Retrieved 2018-07-09.
  4. "Biotech & Pharma". Cluster Gesundheitswirtschaft Berlin-Brandenburg (in German). Retrieved 2018-07-09.
  5. "– Researchers – Molecular Biology & Integral Biomathics". molbio2math.org. Retrieved 2021-06-12.