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Category: biotech/medical – Page 11

Mitochondrial Respiratory Supercomplex Assembly Factor COX7RP Contributes to Lifespan Extension in Mice

COX7RP is a critical factor that assembles mitochondrial respiratory chain complexes into supercomplexes, which is considered to modulate energy production efficiency. Whether COX7RP contributes to metabolic homeostasis and lifespan remains elusive. We here observed that COX7RP-transgenic (COX7RP-Tg) mice exhibit a phenotype characterized by a significant extension of lifespan. In addition, metabolic alterations were observed in COX7RP-Tg mice, including lower blood glucose levels at 120 min during the glucose tolerance test (GTT) without a significant difference in the area under the curve (AUC), as well as reduced serum triglyceride (TG) and total cholesterol (TC) levels. Moreover, COX7RP-Tg mice exhibited elevated ATP and nicotinamide adenine dinucleotide levels, reduced ROS production, and decreased senescence-associated β-galactosidase levels. Single-nucleus RNA-sequencing (snRNA-seq) revealed that senescence-associated secretory phenotype genes were downregulated in old COX7RP-Tg white adipose tissue (WAT) compared with old WT WAT, particularly in adipocytes. This study provides a clue to the role of mitochondrial respiratory supercomplex assembly factor COX7RP in resistance to aging and longevity extension.

Cancer-promoting DNA circles hitchhike on chromosomes to spread to daughter cells

Small, cancer-associated DNA circles “hitchhike” on chromosomes during cell division to spread efficiently to daughter cells by co-opting a process used to maintain cellular identity through generations, Stanford Medicine-led research has found.

These circles, known as extrachromosomal or ecDNA, are major drivers in human cancers. Blocking their ability to associate with chromosomes causes the loss of the circles during cell division and the death of lab-grown cancer cells. Targeting this weak link in the circles’ proliferation could lead to new classes of cancer therapies, the researchers predict.

“Unfortunately, ecDNAs have developed a crafty mechanism that allows them to wreak havoc on human health,” said professor of pathology Paul Mischel, MD. “They are using nature’s own method of gene expression and cell fate to ensure they are safely distributed into the next generation of cells and not lost into the cytoplasm or extracellular space when a cell divides.”

A BCL-xL/BCL-2 PROTAC effectively clears senescent cells in the liver and reduces MASH-driven hepatocellular carcinoma in mice

Yang, Jn-Simon, He et al. report that the dual BCL-xL/BCL-2 PROTAC 753b is a potent and liver-tropic senolytic, which (unlike other inhibitors of BCL-xL) does not cause severe thrombocytopenia. They evaluate its efficacy in natural aging and in reducing progression from steatotic liver disease to hepatocellular carcinoma, using mouse models.

Researchers confirm new Rickettsia species found in dogs

Researchers from North Carolina State University have confirmed that a species of Rickettsia first seen in dogs in 2018 is a new species of bacteria. The new species, dubbed Rickettsia finnyi, is associated with symptoms similar to those of Rocky Mountain spotted fever (RMSF) in dogs, but has not yet been found in humans.

The work appears in Emerging Infectious Diseases.

Rickettsia pathogens are categorized into four groups; of those, the spotted-fever group Rickettsia (which is transmitted by ticks) is the most commonly known and contains the most identified species. There are more than 25 species of tick-borne, spotted-fever group Rickettsia species worldwide, with R. rickettsii—which causes RMSF—being one of the most virulent and dangerous.

Cell nucleus shape may influence cancer treatment success

Cancer cells with a cell nucleus that is easily deformed are more sensitive to drugs that damage DNA. These are the findings of a new study by researchers at Linköping University in Sweden. The results may also explain why combining certain cancer drugs can produce the opposite of the intended effect. The study has been published in the journal Nature Communications.

A few years ago, a new type of drug was introduced that exploits deficiencies in cancer cells’ ability to repair damage to their DNA. These drugs, called PARP1 inhibitors, are used against cancers that have mutations in genes involved in DNA repair, such as the breast cancer gene 1 (BRCA1).

This gene has such a central role in the cell’s ability to repair serious DNA damage that mutations in it greatly increase the risk of developing cancer, often at a young age. The risk is so high that some women with a mutated BRCA1 gene choose to have their breasts and ovaries surgically removed to prevent cancer.

Plant ‘first responder’ cells warn neighbors about bacterial pathogens

Purdue University researchers found that a subset of epidermal cells in plant leaves serves as early responders to chemical cues from bacterial pathogens and communicate this information to neighbors through a local traveling wave of calcium ions. The properties of this local wave differ from those generated when epidermal cells are wounded, suggesting that distinct mechanisms are used by plants to communicate specific types of pathogen attack, the team reported Dec. 2 in Science Signaling.

The new work from Purdue’s Emergent Mechanisms in Biology of Robustness Integration and Organization (EMBRIO) Institute highlights the importance of calcium ion signatures or patterns in the cytoplasm of cells. Plants and animals use calcium ions to transmit biologically critical sensory information within single cells, across tissues and even between organs.

“When a bacterium infects plant material, or when a fungus tries to invade plant tissue, cells and tissues recognize the presence of an attacker,” said Christopher Staiger, a professor in the Department of Botany and Plant Pathology and Distinguished Professor of Biological Sciences. “They recognize both chemical and mechanical cues. This study is largely about how the chemical cues are sensed.”

Light-activated protein triggers cancer cell death by raising alkalinity

One of the hallmarks of cancer cells is their ability to evade apoptosis, or programmed cell death, through changes in protein expression. Inducing apoptosis in cancer cells has become a major focus of novel cancer therapies, as these approaches may be less toxic to healthy tissue than conventional chemotherapy or radiation. Many chemical agents are currently being tested for their ability to trigger apoptosis, and researchers are increasingly exploring light-activated molecules that can be precisely targeted to tumor sites using lasers, sparing surrounding healthy tissue.

Cancer cells have mitochondria that supply energy for rapid growth and division, but an overly alkaline environment is thought to disrupt mitochondrial function, leading to apoptosis.

A microbial protein called Archaerhodopsin-3 (AR3) may hold the key to alkalinity-induced apoptosis. When exposed to green light, AR3 pumps hydrogen ions out of the cell, increasing alkalinity, disrupting cellular functions, and eventually inducing apoptosis.

Single Nucleotide SMN1 Variants in a Cohort of Individuals With Spinal Muscular Atrophy

Background and ObjectivesSpinal muscular atrophy 5q (SMA) is a motor neuron disorder caused by recessive pathogenic variants in the SMN1 gene, which encodes the survival motor neuron (SMN) protein. While the majority of patients with SMA exhibit…

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