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CARM1 (coactivator-associated arginine methyltransferase 1) belongs to a family of enzymes known as PRMTs (protein arginine methyltransferases), which can introduce arginine methylation. CARM1 is also referred to as PRMT4. Protein methylation, the addition of a methyl group to target proteins, is one type of post-translational modification that can change the function of the target proteins.
CARM1 has been reported to be overexpressed in breast cancer, and its overexpression is associated with high-grade tumors and poorer prognosis. So CARM1-specific inhibitors are considered a promising breast cancer therapy. However, until now only few targets of CARM1 have been identified, and how it recognizes these targets remains unclear.

A study in the Proceedings of the National Academy of Sciences (GRP78 haploinsufficiency suppresses acinar-to-ductal metaplasia, signaling, and mutant-driven pancreatic tumorigenesis in mice) shows that inhibiting a specific protein may be a way to combat the deadly pancreatic cancer.

Pancreatic ductal adenocarcinoma (PDAC), which accounts for 95% of all cases of pancreatic cancer, remains an aggressive type of malignant tumor in need of more effective therapies. The five-year survival rate is only about 5%, though surgery offers the only opportunity for a cure. In the United States alone, PDAC killed 39,590 people in 2014.

Patients with Churg-Strauss Syndrome (CSS) may benefit from an anti-IL5 monoclonal antibody. This is the result of a study (Mepolizumab or Placebo for Eosinophilic Granulomatosis with Polyangiitis) published May 18, 2017 in New England Journal of Medicine.
Churg-Strauss Syndrome (CSS), also known as Eosinophilic granulomatosis with polyangiitis (EGPA), is an extremely rare autoimmune condition marked by blood vessel inflammation. It can impair multiple organ systems, such as the lungs, skin, nerves and stomach. The disease generally affects individuals with a history of asthma or allergies. Asthma, eosinophils, fevers, shortness of breath, cough, wheezing, runny nose, sinusitis, and rashes are common symptoms. Left untreated, the disease can be life-threatening.

Alzheimer's disease (AD) was firstly described and named after a psychiatrist and pathologist Dr. Alois Alzheimer in 1906. It is an irreversible, progressive brain disorder that affects cognitive functions. Symptoms usually starts in patients’ mid-60s, but can also occur earlier. According to estimated, 5 million people in the USA have the disease, for which currently there are no treatments to stop or reverse the progression. Exiting therapies only temporarily improve symptoms. Its incidence is rising in line with the aging population. Mechanisms of AD have yet completely understood.

Published 26 April 2017 in Alzheimer’s Research and Therapy, a new study, carried out by Doris Lambracht-Washington, Min Fu, Pat Frost and Roger Rosenberg at UT Southwestern Medical Center, now reports a DNA vaccine that could protect against toxic proteins associated with AD. The researchers demonstrated that a DNA Aβ42 trimer vaccine led to high levels of antibody responses in rhesus macaques.

In the past, there are limited treatment options for people with advanced kidney cancer. These patients tend to have poor outcomes. In recent years, the emergence of novel combination treatments, such as the combination of nivolumab and ipilimumab, have prolonged the survival of some patients. However, there are a still a subpopulation of patients who do not respond to these combination treatments.
Nivolumab is a human IgG4 anti-PD-1 monoclonal antibody used in the treatment of several cancers such as inoperable or metastatic melanoma, metastatic squamous non-small cell lung cancer, primary or metastatic urothelial carcinoma, and renal cell carcinoma. It works by blocking a signal that would have prevented activated T cells from attacking the cancer. Ipilimumab is a also monoclonal antibody and it activates the immune system by a protein that downregulates that immune system, CTLA-4. (Cusabio offers polyclonal antibody.)

Since 2014, the lethal Ebola virus has swept many countries on the planet, particularly Liberia, Sierra Leone, and Guinea in West Africa. Ebola becomes an emerging infectious disease for which there is no known cure. Now, making progress toward a vaccine and therapy against Ebola, researchers reporting in Cell have identified natural human antibodies with the potential to provide broad protection against Ebolaviruses.
Therapies based on monoclonal antibody has shown promise for treatment of Ebola infections. However, one thing that limits their application is that most antibody therapies target just one specific ebolavirus due to their species-specific recognition of the viral glycoprotein (GP). One experimental therapy called ZMappTM, which comprises thress chimeric monclonal antibodies, is specific for Ebola virus, or called Zaire ebolavirus, but is ineffective against two other ebolaviruses known as Sudan virus and Bundibugyo virus. (CusAb strives to provide the excellent products such as Biotin conjugated antibody for researchers.)

PD-1, a 55 kDa transmembrane protein, is an immune checkpoint receptor expressed by activated T cells, B cells, and myeloid cells. It is important for the induction of immune tolerance. Mice lacking PD-1 exhibit a breakdown of peripheral tolerance and show multiple autoimmune features. Tumor cells often express elevated levels of PD-L1, which is the ligand for PD-1, and this help them to evade the body’s immune attacks. Monoclonal antibodies targeting PD-1/PD-L1 interaction are promise in treating various cancers. These antibodies have already been known to unleash T cells, but how they affect macrophages remains unclear. (Cusabio offers Biotin conjugated antibody.)

Now, researchers from Stanford University School of Medicine, University Hospital Basel, and Yale University School of Medicine have found that those antibodies also prompt immune cells to engulf and devour cancer cells. In a paper published online 17 May 2017 in Nature, the researchers report how they made the discovery, which will expand the use of PD-1/PD-L1 blockade antibodies in cancer treatment.

Investigators from Germany have revealed the protective role of a protein in inflammatory bowel disease (IBD). The protein, called CD14, could be targeted to treat or prevent this debilitating and even life-threatening disease.

Inflammatory bowel disease (IBD), a group of diseases that involve inflammation of part or all of the digestive tract and predominantly include ulcerative colitis and Crohn disease, is a result of genetic, microbial, and environmental factors. Many genetic loci have been implicated in IBD development in both humans and mouse models. In particular, a gene called Cd14, which encodes the CD14 protein, has been suggested to be a candidate gene for IBD susceptibility.

Liver disease, which includes is more than a hundred different kinds of diseases of the liver, constitutes one of the most common causes of death worldwide. In Australia alone, approximately 6 million people are suffering from liver disease, putting an enormous burden on the health care system. It is imperative to develop more effective therapeutic agents for liver disease.

One type of liver disease, hepatitis, is an inflammation of the liver tissue. It is most frequently caused by viruses, although the condition can also be caused by other factors, such as heavy alcohol use, certain medications, toxins, other infections, and autoimmune diseases. Over time, hepatitis may progress to liver fibrosis, cirrhosis, liver failure, and liver cancer.

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease and motor neurone disease (MND), is a fatal disorder of motor neurons. It is the most common adult-onset motor neuron disease and is characterized by progressive paralysis and death. Currently, no treatment substantially slows disease progression. The etiological underpinnings of ALS are complex and not fully understood. A lot of genes have been implicated in ALS, including C9orf72, SOD1, TARDBP, and FUS, which are key to the normal function of motor neurons and other cells.

Now a new study shows that a variant in UBQLN4 gene is associated with ALS. The study, led by Dr Yongchao Ma from Northwestern University Feinberg School of Medicine, reveals that UBQLN4 gene variant disrupts a pathway that drives motor neuron development.