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Molecular & Cell Biology

Category: Molecular & Cell Biology


Graphic of microtubules, the 'railway network' within every cell of the human body
Researchers from the University of Warwick have discovered how cells in the human body build their own 'railway networks', throwing light on how diseases such as bowel cancer work. The results have just been published in Nature Scientific Reports.

A new imaging technique has allowed researchers at North Carolina State University, the University of North Carolina at Chapel Hill, and the University of Pittsburgh to see how DNA loops around a protein that aids in the formation of a special structure in telomeres. The work provides new insights into the structure of telomeres and how they are maintained.

If you're fat, can you blame it on your genes? The answer is a qualified yes. Maybe. Under certain circumstances. Researchers are moving towards a better understanding of some of the roots of obesity.

Supposed "junk" DNA, found in between genes, plays a role in suppressing cancer, according to new research by Universities of Bath and Cambridge. The human genome contains around three metres of DNA, of which only about two per cent contains genes that code for proteins. Since the sequencing of the complete human genome in 2000, scientists have puzzled over the role of the remaining 98 per cent.


The scientists found that genome instability increases in cells as XPG levels decrease. The green spots mark locations of DNA double-strand breaks.
If you have a soft spot for unsung heroes, you'll love a DNA repair protein called XPG. Scientists from the U.S. Department of Energy's Lawrence Berkeley National Laboratory (Berkeley Lab) discovered that XPG plays a previously unknown and critical role helping to maintain genome stability in human cells. Their findings also raise the possibility that the protein helps prevent breast, ovarian, and other cancers associated with defective BRCA genes.

It is well known that a predisposition to adiposity lies in our genes. A new study by researchers at the Max Planck Institute of Immunobiology and Epigenetics in Freiburg now shows that it is also crucial how these genes are regulated. The scientists led by Andrew Pospisilik discovered a novel regulatory, epigenetic switch, which causes individuals with identical genetic material, such as monozygotic twins, to either be lean or obese. Interestingly, much like a classical light switch there are only two discrete outcomes -- ON and OFF, or rather obese and not obese -- not continuous increments as with a dimmer. These new insights fundamentally alter our understanding of how epigenetics influences gene outcomes.

A team of scientists has uncovered greater intricacy in protein signaling than was previously understood, shedding new light on the nature of genetic production.

The immune system exercises constant vigilance to protect the body from external threats--including what we eat and drink. A careful balancing act plays out as digested food travels through the intestine. Immune cells must remain alert to protect against harmful pathogens like Salmonella, but their activity also needs to be tempered since an overreaction can lead to too much inflammation and permanent tissue damage.


A histological section of a heart.
Researchers at the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) have identified how two proteins control the growth of the heart and its adaptation to high blood pressure (hypertension). Lead investigator Dr. Guadalupe Sabio explains that the results, described in Nature Communications, not only increase our understanding of the mechanisms used by cardiac cells to grow and adapt, but could also help in the design of new strategies to treat heart failure caused by excessive growth of the heart. The study, carried out by Dr. Sabio and CNIC investigator Bárbara Gonzalez-Terán, shows for the first time that two proteins, p38 gamma and p38 delta, control heart growth.

This meeting will focus on the genetics, biochemistry, and biology of Krüppel-like factors (KLFs) as well as their structurally and functionally related, Specificity Proteins (Sps) along with their impact on human diseases. Significant efforts will be given to discussing the application of KLF/SP-based tools to gene editing and cell-based therapies for regenerative medicine (iPS cells). KLFs/SP proteins constitute a single family of zinc finger-containing transcription factors that exhibit homology to the Drosophila gap gene product, Krüppel. There are at least 18 KLFs and 9 Sp proteins, with a multitude of important functions including regulation of proliferation, differentiation, inflammation/immunity, metabolism, and carcinogenesis. Dysregulation of KLF/SP-mediated pathways contributes to pathological states such as obesity, cancer, and inflammatory conditions. Recent studies indicate that many of these transcription factors have the ability to reprogram somatic cells to inducible pluripotent stem (iPS) cells, and to maintain the pluripotent state of embryonic stem cells; interestingly, several members can substitute for one another in establishing and/or maintaining pluripotency. This transformational discovery has elicited the attention of investigators and medical practitioners from the field of Regenerative Medicine. Molecular insights derived from zinc finger-DNA interactions, which have been derived and most thoroughly validated from work on Sp/KLF proteins has given rise to a new area of research that is growing exponentially, namely gene-editing by artificial KLF-like zinc finger proteins that allow for in vivo gene mutation, mutation repair, deletions, insertion and other type of engineering for both research and medical practice. Thus, the scope and the impact of our 2016 meeting, we will have investigators that discuss the use of Zinc finger nucleases, TALENS, and CAS/CRISPR systems. Lastly, many additional and novel roles for various Sp/KLFs in normal and disease states are only now being fully studied and explored. We expect that through the interaction fostered in this meeting will fuel subsequent collaborations, lead to the design of new diagnostic and therapeutic approaches for broad array diseases. This is truly and international meeting which counts with a confirmed list of speakers from USA, Canada, Europe, and Asia. A large number of oral presentations will be selected from the abstracts, and the selected talks, poster presentations, and recreational activities will provide students and postdoctoral fellows opportunities to exchange ideas and formulate new collaborations.

Cancers evolve over time in patterns governed by the same natural laws that drive physical and chemical processes as diverse as the flow of rivers or the brightness of stars, a new study reports.


A new study from The Scripps Research Institute and Duke University Medical Center reveals the three-dimensional structure of a crucial ion channel
Many cells have microscopic gates, called ion channels, which open to allow the flow of ions across the cell membrane. Thanks to these gates, cells can detect stimuli such as heat, pain, pressure and even spicy food.

When it comes to genes associated with cancer, none have been studied more extensively than p53, a tumor suppressor gene that serves as the guardian of our genetic information. More than half of all cancers have mutations of p53, meaning that this particular gene must often be suppressed in order for a cancer to grow and spread.


Pulmonary neuroendocrine cells (red) are rare cells found in clusters along the mammalian airway, where they act as sensors, sending information to the central nervous system. These clusters are found...
An uncommon and little-studied type of cell in the lungs has been found to act like a sensor, linking the pulmonary and central nervous systems to regulate immune response in reaction to environmental cues.


Researchers counted cells in plates, using different solutions in each plate, to determine changes in cells.
A team of researchers from Colorado State University has been studying DNA damage in living cells to learn more about how genetic abnormalities arise. It has long been known that DNA molecules in every cell get constantly damaged by things from the outside environment, like sunlight, cigarette smoke and radiation. However, more recently researchers have discovered that sources from within the cell itself can sometimes be even more damaging.

Princeton University researchers have captured among the first recordings of neural activity in nearly the entire brain of a free-moving animal. The three-dimensional recordings could provide scientists with a better understanding of how neurons coordinate action and perception in animals.

Molecular biologists at UT Southwestern Medical Center have identified a gene called NORAD that helps maintain the proper number of chromosomes in cells, and that when inactivated, causes the number of chromosomes in a cell to become unstable, a key feature of cancer cells.


In the stem of the Arabidopsis plant, the light-sensitive receptor CRY2 (yellow) spurs a plant to begin a growth cycle and avoid shade.
Despite seeming passive, plants wage wars with each other to outgrow and absorb sunlight. If a plant is shaded by another, it becomes cut off from essential sunlight it needs to survive.


The genetic switch known as NFkB-DNA-IkB. Rice University researchers discovered details of its molecular stripping mechanism through computer models of its energetic transformation.
Rice University researchers have a new twist for those clinging to old ideas about a basic biological process.


When the researchers reduced the activity of TET enzymes in developing granule cells, it impaired the cells' ability to form connections.
From before birth through childhood, connections form between neurons in the brain, ultimately making us who we are. So far, scientists have gained a relatively good understanding of how neural circuits become established, but they know less about the genetic control at play during this crucial developmental process.


This is a 3-D model of the protein complex mTORC1.
For a long time it has been known that the protein TOR - Target of Rapamycin - controls cell growth and is involved in the development of diseases such as cancer and diabetes. Researchers at the University of Basel's Biozentrum together with scientists from ETH Zurich have now examined the structure of mammalian TOR complex 1 (mTORC1) in more detail. The scientists have revealed its unique architecture in their latest publication in "Science".


Graphic shows the structure of diacylglycerol kinase (DgkA) determined with the Free Electron Laser (FEL) in Stanford, Ca.
Scientists have drawn up molecular blueprints of a tiny cellular 'nanomachine', whose evolution is an extraordinary feat of nature, by using one of the brightest X-ray sources on Earth.


Loss of TET function contributes to skewing blood stem cells in favor of forming myeloid cells over other blood cell types by regulating the expression of lineage-specific genes.
Members of the TET (short for ten-eleven translocation) family have been known to function as tumor suppressors for many years, but how they keep a lid on the uncontrolled cell proliferation of cancer cells had remained uncertain. Now, researchers at the La Jolla Institute for Allergy and Immunology demonstrate that TET proteins collectively constitute a major class of tumor suppressors and are required to maintain genome instability.

When researchers looked at different areas within an individual rectal cancer sample, they found cases in which each area contained different genetic mutations. The findings could have significant implications for treatment recommendations.

A particular location in DNA, called the Dlk1-Gtl2 locus, plays a critical role in protecting hematopoietic, or blood-forming, stem cells--a discovery revealing a critical role of metabolic control in adult stem cells, and providing insight for potentially diagnosing and treating cancer, according to researchers from the Stowers Institute for Medical Research.


Tufts biologists induced one species of flatworm -- G. dorotocephala, top left -- to grow heads and brains characteristic of other species of flatworm, top row, without altering genomic sequence.
MEDFORD/SOMERVILLE, Mass. (November 24, 2015)--Biologists at Tufts University have succeeded in inducing one species of flatworm to grow heads and brains characteristic of another species of flatworm without altering genomic sequence. The work reveals physiological circuits as a new kind of epigenetics - information existing outside of genomic sequence - that determines large-scale anatomy.


Location of topologically associated domains (TAD) in the cell nucleus is shown.
Chromosome is a structure inside the cell nucleus that carries a large part of the genetic information and is responsible for its storage, transfer and implementation. Chromosome is formed from a very long DNA molecule - a double chain of a plurality of genes. Given that the diameter of the cell nucleus is usually around hundredth of a millimeter or even less, while the total length of DNA constituting human genome is about two meters, it is clear that DNA must be packaged very tightly.

Scientists at the Institute of Molecular Biology (IMB) in Mainz have unraveled a complex regulatory mechanism that explains how a single gene can drive the formation of brain cells. The research, published in The EMBO Journal, is an important step towards a better understanding of how the brain develops. It also harbors potential for regenerative medicine.

Proteins inside bacteria cells engage in "search-and-rescue"-type behavior to ferret out mismatched DNA and fix it to thwart dangerous mutations that can be associated with certain cancers, a University of Michigan study found.

Scientists at the Institute of Molecular Biology (IMB) have been able to see, for the first time, the dramatic changes that occur in the DNA of cells that are starved of oxygen and nutrients. This starved state is typical in some of today's most common diseases, particularly heart attacks, stroke and cancer. The findings provide new insight into the damage these diseases cause and may help researchers to discover new ways of treating them.

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