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Research reveals the brain roots of Parkinson disease

Posted by star on 2019-09-18 18:37:36

Researchers at Washington university school of medicine in St. Louis identified the earliest signs of Parkinson's disease in the brain before patients developed Parkinson-related symptoms. The findings, published in the journal Cell, suggest a new view of the disease and could lead to the development of screening tools to identify the most at risk.
Parkinson's disease is the second most common neurodegenerative disease after Alzheimer's. The disease is characterized by motor and cognitive problems that start in the brain long before a patient is diagnosed. The early stages of Parkinson's disease are critical, and treating it as early as possible may slow its progress.
The new study is the first to demonstrate the key role of the brain chemical serotonin in the early stages of Parkinson's disease. The results suggest that systemic changes in serotonin may be an important warning sign of the disease.
The researchers said: "traditionally, Parkinson's disease is caused by damage to the dopamine system, but we found that changes in the serotonin system occur first, before patients begin to show symptoms. "The results suggest that early changes in the serotonin system could provide insights into new treatments that could slow the progression of Parkinson's disease and ultimately stop it."
α-Synaptic nuclein (SNCA) is present in the brain of Parkinson's disease patients. People with mutations in theα-Synuclein gene are extremely rare, but they are almost certain to develop Parkinson's disease, making them a prime candidate for Parkinson's research. The researchers compared 20 patients with a mutation in the synaptic nuclein gene with 20 healthy volunteers and found that the serotonin system in Parkinson's patients began to malfunction before symptoms that affect movement began.
Lead author Heather Wilson said: "we found that serotonin function is an important marker for the development of Parkinson's disease. And we found detectable ......

Human - virus protein interactions

Posted by star on 2019-09-17 23:05:18

A virus is a much smaller infectious organism than a bacterium. To survive, it must find a suitable host to live inside and use protein-protein interaction (PPI) to dominate the host cell's survival function and absorb nutrients. In turn, host cells use PPI to activate innate antiviral defenses and adaptive immune systems to control viral replication. But in this battle, once the host cell fails to stop the virus from replicating, the large number of "parasitic" viruses that rapidly multiply in its body will tilt out and start a new "parasitic" journey, infecting more healthy cells.
Therefore, knowledge of protein-protein interactions (PPI) is crucial to understanding the relationship between viruses and their hosts. Currently, scientists mainly study protein-protein interactions through high-throughput methods. Although many new discoveries have been made, the lack of scalability of this method also limits further studies. To this end, the researchers developed a new computing framework called P-HIPSTer. It can use the information of protein structure to predict the interaction between virus protein and human protein, which can effectively compensate for the lack of scalability of high-throughput method.
The researchers say p-hipster has been used to study more than 2,000 known viruses that infect humans and about 23,000 proteins that encode them. The algorithm predicted about 385,000 possible interacting protein pairs with an accuracy of nearly 83 percent, creating a small database of human-virus protein interactions. It has contributed to the further research of human immunology and infectious diseases.
Dr. Sagi Shapira, a professor in the department of microbiology and immunology at Columbia University, who led the study, said the database of human-viral protein interactions created by the institute could help scientists break through current research bottlenecks to better understand viral and human protein interactions. Next, P-HIPSTer will be......

Classification and study of cyclin dependent kinases

Posted by star on 2019-09-16 19:24:37

The cell cycle is an important part of cell life. Studies have found that the occurrence of various malignant tumors is closely related to the disorder of cell cycle regulation mechanism, so tumor is also considered as a cell cycle disease. Cyclin dependent kinase (CDK) promotes the orderly progression of the cell cycle, so cyclin dependent kinase inhibitors (CDKI) block the cell cycle and control cell proliferation, resulting in anti-tumor activity.
CDK is a serine/threonine kinase with short n-terminal and long C-terminal, and its ATP-binding pocket is located between n-terminal and c-terminal. CDK functions at all stages of the cell cycle, promoting orderly cell proliferation. Unlike other kinases, CDK must bind to cyclins to function. The periodic expression and degradation of cyclin promote the orderly progress of cell cycle and cause cell growth and proliferation.

CDKI works by competitively binding ATP binding regions of CDK, which can effectively prevent cell proliferation or promote cell apoptosis. At present, some researches on CDKI have entered clinical stage.
According to the different selectivity of CDKI to target enzymes, it can be divided into three categories:
(1)broad-spectrum CDKI can prevent cell from G1 phase to S phase and G2 to M phase transition, at the same time can interfere with the RNA polymerase Ⅱ role in transcription process.
(2) Specific CDKI is a small molecule with high selectivity, which can inhibit CDK2/cyclinA. The specific mechanism of CDKI is to block cell cycle by inhibiting gene transcription.
(3) CDK inhibitors with other kinase activities have been found in the treatment of non-small cell carcinoma to effectively inhibit the proliferation of tumor cells. The mechanism of anticancer effect may be based on the influence on the ......

YAP1 is a potential target for the treatment of lung cancer

Posted by star on 2019-09-11 19:09:29

Cancer stem cells are a group of special cells in a tumor that initiate and maintain the development of cancer through self-renewal and differentiation. These cells are equivalent to the "seeds" of cancer, which not only support the growth of tumors, but also promote tumor metastasis and recurrence.
YAP1 protein can promote the growth of lung cancer cells, but the mechanism of action of this protein was not known at the time. Researchers at the Moffitt Cancer Center have found that YAP1 plays an important role in the self-renewal of cancer stem cells.
The study showed that effects of YAP1 were mediated through the embryonic stem cell transcription factor, Sox2. YAP1 could transcriptionally induce Sox2 through a physical interaction with Oct4; Sox2 induction occurred independent of TEAD2 transcription factor, which is the predominant mediator of YAP1 functions. The binding of Oct4 to YAP1 could be detected in cell lines as well as tumor tissues; the interaction was elevated in NSCLC samples compared to normal tissue as seen by proximity ligation assays. YAP1 bound to Oct4 through the WW domain, and a peptide corresponding to this region could disrupt the interaction. Delivery of the WW domain peptide to stem-like cells disrupted the interaction and abrogated Sox2 expression, self-renewal, and vascular mimicry.
The researchers compared the levels of YAP1 and OCT4 in lung cancer and normal tissues. They found higher levels of YAP1 and more interaction with OCT4 in primary and metastatic lung tumors. Patients with high YAP1 levels in the tumor have a worse prognosis than those with low YAP1 levels. These findings suggest that YAP1 can be a potential target for the treatment of lung cancer.
Studies have shown that blocking YAP1 can inhibit stem cell self-renewal, prevent them from forming a blood vessel-like structure, and reduce the growth of lung cancer cells in mice.
"Inhibition of YAP1 function or interference with the binding of YAP1 to O......

Russian scientists have created a genetic model to help understand how the body suppresses autoimmune and neoplastic diseases. The scientists studied the properties of the Foxp3 protein which is responsible for Treg cell development and normal function. They found that removal of the Foxp3 protein gene from genomic DNA blocks Treg cell development and leads to biological death.
Many autoimmune diseases are associated with Foxp3 synthesis and abnormal numbers of Treg cells. The Foxp3 protein does not act alone, but as part of a protein complex that serves the genes essential for normal functioning of Treg cells. This group of proteins also includes Foxp1.
The researchers established a genetic model to explain how Foxp1 affects Foxp3. They first removed part of the Foxp1 gene from Treg from experimental mice. Comparing "normal" cells with Foxp1-depleted cells, it was found that Foxp3 has a much poorer ability to bind DNA without Foxp1. That means protein-coding genes that are critical for the normal function of Treg cells do not work properly without Foxp1. Therefore, Foxp3 is required for Treg, and Foxp1 is also very important, there is a negative impact on Foxp3 if the Foxp1 is removed. Understanding the structure of protein complexes composed of Foxp1 and Foxp3 is the key to making drugs that selectively affect Treg cells.
"The results broaden our understanding of the molecular mechanisms that regulate immune tolerance, which can be used to treat cancer and autoimmune diseases," the researchers said. "Cancerous tumors attract Treg cells to protect themselves from the body's immune system. The more Treg cells in a tumor, the worse the patient's prognosis. Therefore, if we can control the number and activity of Treg cells, we can reduce them in the tumor and increase them in the case of autoimmune diseases. It is possible to create safe drugs to treat diseases that have not been cured so far."
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