The mechanisms by which cells are used to discover and remove organelles

Through research involving recombinant horse proteins, researchers at UT Southwestern Medical Center have discovered the mechanisms by which cells are used to discover and remove organelles. They are known as mitochondria. When these organelles are damaged, it can cause genetic problems such as cancer, neurodegenerative diseases, inflammatory diseases and aging. Dr. Beth Levine, director of the UT Southwestern Automation Research Center and Dr. Beth Levine, a senior author of the study, said in a recent presentation that understanding how the process works may lead to new treatments to prevent certain diseases and even certain aspects of aging. The Autophagy Research Center is the only autophagy research center in the country.

Because mitochondria are high in energy, when they are damaged, toxic chemicals that release reactive oxygen species are released to the rest of the cell. Removal of damaged mitochondria by autophagy, known as mitochondrial autophagy, is important for cellular health. Researchers have noted that the discovery of tag proteins on the mitochondrial outer membrane - specifically the Parkin- proteins attached to these tags - explains cell degrading organelles, called autophagosomes, and it targets to pathological mitochondria.

In the study, the researchers found a protein present on the mitochondrial membrane prohibitin 2 (PHB2), but PHB2 was exposed to the damaged mitochondrial outer membrane. Once the cells break, the protein LC3 in the autophagy outside the role of monitoring, and LC3 will be attracted to the PHB2 protein. The LC3 protein then attaches to PHB2, and the autophagosome carries the damaged organelle to the lysosome - another organelle found in the cell, acting like a tiny stomach with enzymes that break down cell waste.

"This study found that PHB2 is critical for targeted mitochondrial autophagic degradation," said Dr. Levine, "Previous studies have linked the presence of PHB2 to the prevention of cancer, aging, neurodegeneration, and inflammation. Significantly, the key role of PHB2 is to help to get rid of damaged mitochondria in cells, playing a catalytic role."

The study also found that PHB2 is necessary to routinely remove the maternally-derived mitochondrial DNA from the developing embryo, leaving only maternal DNA from the mother. This is a work done in roundworms, but there is a recent study conducted in mice using a mouse model elsewhere suggesting that mitochondria are also used to remove paternal mitochondria in mammalian embryos," said Dr. Wu Chung, a postdoctoral fellow at UT Southwestern, the first author of the study.

"Typically, only maternal mitochondrial DNA is passed on to offspring," Dr. Levine said. For unknown reasons, the presence of paternal mitochondrial DNA predicts some genetic or health problems in the offspring. In another finding, the UTSW study showed that PHB2 is essential for the Parkin effect, although scientists are paying more attention to Parkin's role in supporting autophagic PHB2. Flarebio offers superior recombinant proteins including recombinant Cd44 at good prices.

The mechanism of cancer tumor cells becoming cancer stem cells that can sustain long-term growth

International research, led by scientists from the London Creek Institute and the Hebrew University of Jerusalem, sheds light on the survival mechanisms in cancer cells that can re-emerge even after aggressive treatment. In a paper published in Science which also publishes some other studies on recombinant human proteins, the researchers describe the mechanism by which cancerous tumor cells become cancer stem cells that can sustain long-term growth.

When cancer develops, the resulting cells are heterogeneous in their biological properties and have different contributions to tumor development. Only a small percentage of cancer cells can form new tumors or metastases, and these are called "cancer stem cells". This difference between tumor cells constitutes a major challenge in understanding the nature of the tumor, its sensitivity to drugs and the effective treatment of all tumor cells.

"Many chemotherapeutic agents leave a small amount of cancer stem cells, causing disease to re-emerge after a few years," said Eran Meshorer, director of the Stem Cell and Epigenetics Laboratory of the Life Sciences Institute. "Therefore, it is important to identify cancer stem cells and characterize the differences between different tumor cells as a basis for detection of weaknesses during disease progression."

Cancer stem cells are not limited to the tumor itself. They can re-engage in a healthy environment and stimulate the disease. In order to study the characteristics of these unique cells, Prof. Dr. Meshorer and Dr. Alva Biran from the Hebrew University collaborated with Dr. Paula Scaffidi and Dr. Christina Morales Torres from the Crick Institute in London. The international team also includes Dr. Ayelet Hashahar Cohen of the Hebrew University, Dr. Rotem Ben-Hamo and Sol Efroni of Bar-Ilan University and Dr Tom Misteli of the NIH National Cancer Institute.



The team found that in many cancer types, those cancer stem cells lost one of their DNA packaging proteins, H1.0. By binding to DNA, the H1.0 gene was expressed.

"In order to understand the mechanism of action, we mapped the interaction pattern with DNA and found that it binds to the regulatory region of the gene," explained Professor Meshorer. "When the levels of H1.0 increase, these genes can inhibit the proliferation of cancer cells."

The study is based on epigenetics - a scientific field that investigates gene expression by switching the DNA on and off genes. To identify cancer stem cells from other cells in the tumor, the team studied the epigenetic mechanisms that differentiate at least sorted cells with infinite splitting properties and the potential to produce growth, as well as more sorted cells lacking this ability.

The results show an inverse relationship between H1.0 and cancer cell division: with the decrease of H1.0 levels, the greater the potential for uncontrolled division of the cells is. In contrast, high levels of protein prevent this process. We found that the disappearance of H1.0 protein is the characteristic of cancer stem cells, and it is necessary to maintain the ability to divide and the potential for growth.



This finding opens the door to medical intervention for cancer stem cells, aimed at restoring high levels of H1.0 in all cancer cells and blocking the differentiation of cancer cells. Although further research is needed to understand the usefulness of H1.0 protein in preventing cancer growth and spread, this study significantly expresses the cancer stem cell mechanism and relatively new epigenetic approaches to cancer research. Flarebio offers recombinant proteins of good quality such as recombinant Cd44 at good prices.

How do plant seeds fool beetles?

We have seen many animals survive by being camouflaged to avoid being eaten by their predators. But have you seen any plants protect themselves by mimicry? A team consisted of researchers from both University of Cape Town and the University of KwaZulu-Natal in South Africa, has found an example of that - a seed from a plant uses mimicry to fool a beetle. They published their paper in the journal Nature Plants, which also have other studies on recombinant rat proteins. In their paper they describe the relationship between the seeds and the beetles and the deceptive dispersal they witnessed through observation.

In fact, many examples of animals or plant mimicry have been noted and reported in studies published before, but until now, no examples of a plant using mimicry to disperse seeds have been documented. The research which seeds of a grassy plant known as Ceratocaryum argenteum were somehow dispersed used to draw public attention, but no one had figured out how it was occurring. The researchers write that they believed it was because mice carried them about. To make sure about the guess, they dropped 195 of the seeds near monitoring stations in De Hoop Nature Reserve and recorded what happened with video cameras.

Over a single day, dung beetles moving through the area had grabbed nearly half of the seeds and rolled them to nearby locations where they buried them later. As you know, dung beetles normally grab animal droppings and bury them for eating or use them for a place to lay eggs.

Subsequently, the researchers dug up all the seeds which were buried by the beetles and found no traces of beetles around, let alone any eggs laid by dung beetles. The results suggested that those beetles discovered the ruse as they attempted to eat them or lay eggs. Therefore, the team guessed that the dung beetles had been fooled into carrying the seeds to a distant places and planting them and got no reward for their efforts.

They inspected the seeds and found that they looked like bontebok dung a lot. What's more, the chemical composition of the seeds closely resembled dung as well. It must be the smell of the seeds that fools the beetles. Flarebio provides you with superior recombinant proteins including recombinant Cd44 at competitive prices.

The problem of plants facing with high salt can be saved by some newly-found proteins

Previous studies show that high salt in soil dramatically stresses plant biology and reduces the growth and yield of crops. A study led by professor Staffan Persson who is interested in producing recombinant proteins like recombinant rat proteins, from University of Melbourne, Australia, formerly at the Max Planck Institute of Molecular Plant Physiology, found specific proteins that allow plants to grow better under salt stress, and may help breed future generations of more salt-tolerant crop plants.

Humans can move away from the salty snacks or drink more water, but if a plant is stuck in high salt (or saline) soils, it must use other tactics to cope. More and more of the world' crops are facing salt stress with high salt in soils (also known as salinity) affecting 20% of the total, and 33% of irrigated, agricultural lands worldwide. We need to increase production of food by 70% to feed an additional 2.3 billion people by 2050. Salinity is a major limiting factor for this goal as more than 50% of the arable land may be salt afflicted by the year 2050. Thus finding genes and mechanisms that can improve plant growth under such conditions is of utmost urgency.

"Plants need to make bigger cells and more of them if they want to grow and develop, " said Prof Persson, which is good at producing recombinant proteins like recombinant horse proteins.

"Unlike animal cells, plant cells are surrounded by a cellular exoskeleton, called cell walls which direct plant growth and protect the plant against diseases. Importantly, most of the plants biomass is made up of the cell wall with cellulose being the major component. Hence, plant growth largely depends on the ability of plants to produce cell walls and cellulose, also under stress conditions, and it is therefore no surprise that research on cell wall biosynthesis is of high priority."

The present study shows that an previously unknown family of proteins supports the cellulose synthase machinery under salt stress conditions, and was named "Companions of Cellulose synthase (CC). These CC proteins are part of the cellulose synthase complex during cellulose synthesis. The researchers found that the CC gene activity was increased when plants were exposed to high salt concentrations.

"In an additional step, we made fluorescent versions of the CC proteins and observed, with the help of a special microscope, where and how they function. It was quite a surprise to see that they were able to maintain the organization of microtubules under salt stress. This function helped the plants to maintain cellulose synthesis during the stress", said Dr. Anne Endler, co-first author of this study.

The research group proved that the plants lacking the CC activity were unable to maintain their microtubules intact. The loss in microtubule function led to a failure in maintaining cellulose synthesis, which explained the reduction in plant growth on salt.

The results of the study provide a mechanism for how the CC proteins aid plant biomass production under salt stress and help plants to grow on salt. The team has identified a protein family that helps plants to grow on salt, and outlined a mechanism for how these proteins aid the plants to produce their biomass under salt stress conditions. The study was published the day before yesterday in the journal Cell. Flarebio provides good-quality recombinant proteins like recombinant CD44 at competitive prices.

Cancer cells: the new discovery of PITPNC1 protein

Researchers from Rockefeller University at New York and the University of Bergen at Norway published their discovery of a protein called PITPNC1 on the journal Cancer. Molecular biologist at the University of Bergen, first author Dr. Nils Halberg who is interested in producing recombinant proteins like recombinant dog proteins said, "We found that invasive cancer cells spreading in colon, breast and skin cancer have higher content of PITPNC1 protein than non-invasive cancer cells."

More than 90% of cancer deaths are due to metastasis, namely so-called new tumor lesions caused by the condition that invasive cells leave the primary tumor and metastases to other parts of the body. Any discoveries about the metastasis process of cancer cells all help us step further on the way of saving millions of lives.

The name of metastatic cancer cells is the same with that of the cancer cells it comes from. For example, lung metastatic cancer forming by a kind of breast tumor metastasis is known as metastatic breast cancer, instead of lung cancer. Under a microscope, metastatic tumor cells generally look very similar to primary cancer cells. Moreover, metastasis cancer cells and primary cancer cells often have some similar molecular features, such as the expression of certain proteins. It can be proved by many recombinant proteins such as recombinant rat proteins.

Dr. Halberg explained that there are many different kinds of cells inside a tumor cell. Some of the cells are benign and will not cause any troubles, while some cells become invasive and are ready to spread at any time. And it is difficult to predict which cells are about to become invasive cells.

In their paper, the team describes how they separated invasive cells from the metastatic breast cancer, melanoma and colon cancer and how they found that the invasive cells all express a kind of genes more highly than cells without proliferation. The gene encodes the protein PITPNC1. Dr. Halberg said, "This means that we can make a forecast about which tumor cells are easy to become invasive and spread at an earlier stage than what we can do currently."

He and his colleagues also found that this protein also has a very specific function in the process of cancer spread. It can make of blood vessels to metastase tumor cells to new sites in vivo. In order to be able to leave the tumor and enter blood vessels and then adhere to a new organ, invasive cells need to penetrate tissue. Dr. Halberg said that they cut matrix proteins around cells by releasing a kind of molecules like scissors, while it is PITPNC1 protein which regulates this process.

The team hopes that the results would help to find treatment to reduce the risk of proliferation of cancer - for example, after surgery. Halberg concluded, "If we can provide a personalized treatment targeting at this protein, we can prevent the spread of it."

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