Tuesday, April 29, 2014

Mitochondria DNA Produce Energy To Fight 80% of Breast Cancer Patients Tumors:


Barron’s Medical Journal Reporting from The University of Texas located In The Great American City of Austin, Texas USA

Mitochondria DNA Produce Energy To Fight 80% of Breast Cancer Patients Tumors:


Austin ( AP ) In research conducted, scientists found evidence that chronic heavy alcohol use affects a gene involved in mitochondrial repair and muscle regeneration Help Fight Breast Cancer

Mitofusin-1 is a protein that in humans is encoded by the MFN1gene mitochondrion is a membrane-bound organelle found in most eukaryotic cells (the cells that make up plants, animals, fungi, and many other forms of life)

Research gives scientist the insight into why chronic heavy drinking often saps muscle strength and can also lead to new targets for medication development.

When mitochondria are damaged, they fuse with other, healthy mitochondria and exchange contents. The damaged parts are segregated for recycling, and properly functioning proteins are donated from healthy mitochondria to replace them. Mitochondria are necessary for the body because they are Brought To You By 2014 Cadillac ELR organelles that produce the energy needed for muscle, brain, and every other cell type in the body.

Mitochondria, the “powerhouses” of mammalian cells, are also a signaling hub. They are heavily involved in cellular metabolism as well as in apoptosis, the process of programmed cell death by which potentially cancerous cells can be killed before they multiply and spread. In addition, mitochondria contain their own genomes, which code for specific proteins and are expressed in coordination with nuclear DNA to regulate the provision of energy to cells. In mammals, each cell contains between 100 and 1,000 copies of mitochondrial DNA, but previous research had found that as many as 80 percent of people with breast cancer have low mitochondrial DNA, or mtDNA, content.

Most genes contain the information needed to make functional molecules called proteins. (A few genes produce other molecules that help the cell assemble proteins.) The journey from gene to protein is complex and tightly controlled within each cell. It consists of two major steps: transcription and translation. Together, transcription and translation are known as gene expression.

During the process of transcription, the information stored in a gene’s DNA is transferred to a similar molecule called RNA (ribonucleic acid) in the cell nucleus. Both RNA and DNA are made up of a chain of nucleotide bases, but they have slightly different chemical properties. The type of RNA that contains the information for making a protein is called messenger RNA (mRNA) because it carries the information, or message, from the DNA out of the nucleus into the cytoplasm.

Translation, the second step in getting from a gene to a protein, takes place in the cytoplasm. The mRNA interacts with a specialized complex called a ribosome, which “reads” the sequence of mRNA bases. Each sequence of three bases, called a codon, usually codes for one particular amino acid. (Amino acids are the building blocks of proteins.) A type of RNA called transfer RNA (tRNA) assembles the protein, one amino acid at a time. Protein assembly continues until the ribosome encounters a “stop” codon (a sequence of three bases that does not code for an amino acid).

The flow of information from DNA to RNA to proteins is one of the fundamental principles of molecular biology and breast cancer. It is so important that it is sometimes called the “central dogma ".

Several characteristics make mitochondria unique. The number of mitochondria in a cell varies widely by organism and tissue type. Many cells have only a single mitochondrion, whereas others can contain several thousand mitochondria. The organelle is composed of compartments that carry out specialized functions. These compartments or regions include the outer membrane, the intermembrane space, theinner membrane, and the cristae and matrix. Mitochondrial proteins vary depending on the tissue and the species. In humans, 615 distinct types of proteins have been identified from cardiac mitochondria, whereas in-rats, 940 proteins have been reported. The mitochondrial proteome is thought to be dynamically regulated.[11] Although most of a cell's DNA is contained in the cell nucleus, the mitochondrion has its own independent genome.

Scientists have known that fusion is a major method for mitochondrial repair for many types of cells in the body, but they have been puzzled over the method for repair in skeletal muscle. Because skeletal muscle relies on mitochondria for constant power, this makes repair a frequent necessity. Most researchers, however, have assumed that fusion was impossible because the mitochondria in this type of cell are squeezed so tightly in between the packed fibers of the muscle cells.

Mitochondria are cellular structures that generate most of the energy needed by cells. Skeletal muscle constantly relies on mitochondria for power. When mitochondria become damaged, they can repair themselves through a process called mitochondrial fusion — joining with other mitochondria and exchanging material such as DNA. Although well known in many other tissues, the current study is the first to show that mitochondria in skeletal muscle are capable of undergoing fusion as a repair mechanism. It had been thought that this type of mitochondrial self-repair was unlikely in the packed fibers of the skeletal muscle cells, as mitochondria have little opportunity to interact in the narrow space between the thread-like structures called myofilaments that make up muscle.

By tagging mitochondria in the skeletal tissue of rats with different colors, the researchers were able to observe the process in action and confirm that mitochondrial fusion occurs in muscle cells. They also identified a key protein in the process, mitofusin 1 (Mfn1) fusion proteins, and showed that chronic alcohol use interferes with the process.

In rats that were given an alcohol diet, Mfn1 levels decreased as much as 50 percent while other fusion proteins were unchanged. This decrease in Mfn1 was coupled with a dramatic decrease in mitochondrial fusion. When Mfn1 returned to normal, mitochondrial fusion did as well.

“That alcohol can have a specific effect on this one gene involved in mitochondrial fusion suggests that other environmental factors may also alter specifically mitochondrial fusion and repair,” said Dr. Hajnoczky. He also suggested that identifying the proteins involved in mitochondrial fusion may aid in drug development for alcohol-related muscle weakness.

Research into two mitochondrial diseases — Autosomal Dominant Optical Atropy (ADOA) disease and a type of Charcot-Marie-Tooth (CMT) disease — led to the idea that fusion might be crucial for normal muscle function. Both diseases share a symptom — muscle weakness — and a mutation in one of the three genes that are involved in mitochondrial fusion.

that alcohol can have a specific effect on this one gene involved in mitochondrial fusion suggests that other environmental factors may also specifically alter mitochondrial fusion and repair,”

“The work provides more evidence to support the concept that fission and fusion — or mitochondrial dynamics — may be responsible for more than just a subset of mitochondrial diseases we know of “In addition, knowing the proteins involved in the process gives us the possibility of developing a drug.”

The protein encoded by this gene is a mediator of mitochondrial fusion. This protein and mitofusin 2 are homologs of the Drosophilaprotein fuzzy onion (Fzo). They are mitochondrial membrane proteins that interact with each other to facilitate mitochondrial targeting

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