Das genomische Material einer Zelle muss so in einen winzigen Zellkern verpackt werden, dass es einerseits geordnet ist und andererseits nach Bedarf abgelesen, verdoppelt oder repariert werden kann. Für eine platzsparende Verpackung sind Proteine verantwortlich, die die DNA aufrollen oder auch in Schleifen legen können. Die Wissenschaftler Kikuë Tachibana und Karl Duderstadt des Max-Planck-Instituts für Biochemie in Martinsried erforschen die Aufgabe und Funktionsweise dieser molekularen Maschinen. Wie sie herausfinden konnten, spielt der MCM-Komplex eine wichtige Rolle bei der Begrenzung der Schleifenbildung und somit auch bei der dreidimensionalen Struktur des Genoms und der Genregulation.

The entire genomic material of a cell must be packed into a tiny cell nucleus in such a way, that on the one hand, it can be stored in an organized manner and, on the other hand, it can be transcribed, duplicated or repaired as needed. Different proteins are responsible for space-saving packaging, which can roll up or loop the DNA. Scientists Kikuë Tachibana and Karl Duderstadt from the Max Planck Institute of Biochemistry in Martinsried are investigating the exact task and function of these molecular machines. They discovered that the MCM complex plays an important role in restricting DNA loop formation and thus in the three-dimensional structure of the genome and in gene regulation.

Although clinical labs have known for almost a century that a oddly shaped nucleus resembling pince-nez glasses in blood cells could indicate leukemia, the cause of this anomaly remained unknown. Scientists have now discovered that loss of nuclear Lamin B1 induces defects in the nuclear morphology and in human hematopoietic [blood-forming] stem cells associated with malignancy. The scientists went on to detail that lamin B1 deficiency alters genome organization. This in turn causes expansion of blood-forming stem cells, a bias towards their becoming myeloids, genome instability due to defective DNA damage repair and other problems that set the stage for cancer.

Although clinical labs have known for almost a century that a oddly shaped nucleus resembling pince-nez glasses in blood cells could indicate leukemia, the cause of this anomaly remained unknown. Scientists have now discovered that loss of nuclear Lamin B1 induces defects in the nuclear morphology and in human hematopoietic [blood-forming] stem cells associated with malignancy. The scientists went on to detail that lamin B1 deficiency alters genome organization. This in turn causes expansion of blood-forming stem cells, a bias towards their becoming myeloids, genome instability due to defective DNA damage repair and other problems that set the stage for cancer.

Researchers have revealed how an ‚accordion effect‘ is critical to switching off genes, in a study that transforms the fundamentals of what we know about gene silencing. The finding expands our understanding of how we switch genes on and off to make the different cell types in our bodies, as we develop in the womb.

Researchers have revealed how an ‚accordion effect‘ is critical to switching off genes, in a study that transforms the fundamentals of what we know about gene silencing. The finding expands our understanding of how we switch genes on and off to make the different cell types in our bodies, as we develop in the womb.

Researchers have discovered another way tumor cells transfer genetic material to other cells in their microenvironment, causing cancer to spread.

Scientists have identified variants in two genes that are associated with accelerated aging in childhood cancer survivors.

A researcher has made a discovery that alters our understanding of how the body’s DNA repair process works and may lead to new chemotherapy treatments for cancer and other disorders. Researchers discovered that base excision repair has a built-in mechanism to increase its effectiveness — it just needs to be captured at a very precise point in the cell life cycle.

Researchers have developed a new fluorescent label that gives a clearer picture of how DNA architecture is disrupted in cancer cells. The findings could improve cancer diagnoses for patients and classification of future cancer risk.

A new study shows how certain RNA molecules control the repair of damaged DNA in cancer cells, a discovery that could eventually give rise to better cancer treatments.

New proteomics method identifies proteins binding to R-loops and decodes the role of the DDX41 protein in opposing double-strand breaks in the cells‘ DNA

Scientists believe it may be possible to prevent DNA changes driven by two proteins highly active in leukemia and other cancers. They recently reported a new mechanistic target for drug development.

Dresden researchers explain how liquid-like protein droplets collectively read DNA regions to switch on genes.

Dresdner Forscher erklären, wie Proteine in flüssigkeitsartigen Tropfen gemeinschaftlich agieren um Bereiche auf der DNA abzulesen und Gene anzuschalten.

A protein that masterminds the way DNA is wrapped within chromosomes has a major role in the healthy functioning of blood stem cells, which produce all blood cells in the body, according to a new study.

A new study has illuminated an important process that occurs during cell division and is a likely source of DNA damage under some circumstances, including cancer.

Faulty DNA damage repair can lead to many types of cancer, neurodegenerative diseases, and other serious disorders. Investigators have developed high-throughput microscopy and machine learning systems that can identify and classify DNA repair factors. The investigators have identified nine previously unknown factors involved in the process of cellular DNA repair.

Researchers have identified a new mechanism by which a protein known for repairing damaged DNA also protects the integrity of DNA by preserving its structural shape. The discovery, involving the protein 53BP1, offers insight into understanding how cells maintain the integrity of DNA in the nucleus, which is critical for preventing diseases like premature aging and cancer.

There are myriad reasons why cancers develop. By studying genes which are altered in people with lymphoma, a multidisciplinary team of researchers has identified a key mechanism involved in disease development. This signaling pathway, which the researchers describe in detail, controls the repair of DNA damage.

Scientists describe T. adhaerens‘ unusual behavior, including its capacity to repair its DNA even after significant radiation damage and to extrude injured cells, which later die. The findings advance scientific investigations of natural cancer-suppression mechanisms across life. Insights gleaned from these evolutionary adaptations may find their way into new and more effective therapies for this leading killer.

A protein that protects cells from DNA damage, p53, is activated during gene editing using the CRISPR technique. Consequently, cells with mutated p53 have a survival advantage, which can cause cancer. Researchers have found new links between CRISPR, p53 and other cancer genes that could prevent the accumulation of mutated cells without compromising the gene scissors‘ effectiveness.

Findings show that cell-free DNA in cerebrospinal fluid can be used to detect measurable residual disease and identify patients at risk of relapse.

Researchers identified a small RNA molecule called miR-766-5p that reduces expression of MYC, a critical cancer-promoting gene. This microRNA reduces levels of proteins CBP and BRD4, which are both involved in super-enhancer (SE) formation. SEs form in areas of DNA that can fuel MYC expression and tumor progression. This study provides strong evidence for developing miR-766-5p as a novel therapeutic to treat MYC-driven cancers.

Researchers have mapped out how hundreds of mutations involved in two types of cancer affect the activity of proteins that are the ultimate actors behind the disease. The work points the way to identifying new precision treatments that may avoid the side effects common with much current chemotherapy.