This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Cancer involves the reprogramming of the body’s cells to allow them to grow, divide, and travel throughout the body. One of the processes involved – metabolic reprogramming – allows cells to use new energy sources for fuel, switching from oxidative phosphorylation to glycolysis. and enabling tumor cells to grow uncontrolled. A recent study evaluated the involvement of the tumor suppressor gene PTEN in metabolic reprogramming. Researchers compared cancerous and noncancerous liver tissue from 128 patients with hepatocellular carcinoma. They found that in cancerous liver tissue, PTEN had a reciprocal relationship with another protein, PI3K. PTEN was downregulated in HCC tissues, and its loss predicted a poor prognosis. Overexpressing PTEN blocked the switch to glycolysis, while elevated PI3K expression was observed in HCC tissues and was inhibited by PTEN overexpression..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Alzheimer’s disease is the sixth leading cause of death and one of the most prevalent forms of dementia, affecting over 50 million people worldwide. Unfortunately, the molecular signaling pathways underlying neurodegeneration in Alzheimer’s disease are not clearly understood. A recent study identified a link between two physiological phenomena that are affected in Alzheimer's disease: disrupted calcium signaling, which is associated with memory loss and cognitive dysfunction; and increased iron accumulation, which results in neurotoxicity in the brain. Using genetically modified human cell lines and mice, the researchers studied the mechanistic connections between calcium signaling and iron transport. They found that calcium (Ca²⁺) signaling through CAMKK2 and CAMK4 proteins had direct effects on transferrin protein-mediated iron transport..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Just as it does for humans, morning signals the time to wake up for plants. Sunlight triggers stomata, which are tiny pores on plant leaves, to open. This boosts photosynthesis by letting CO₂ in and O₂ out. Cells known as guard cells are the gatekeepers of this process, and opening the stomata requires a lot of energy. But scientists have long wondered where this energy comes from. Because while guard cells serve a key photosynthetic function, they appear less equipped than surrounding cells to perform photosynthesis. Now, researchers from HKU and ETH have discovered guard cells’ secret source of fuel. Experiments on Arabidopsis plants showed that guard cells import most of their energy in the form of sugar from surrounding mesophyll cells. Mesophyll cells contain many more chloroplasts than guard cells, helping them produce large amounts of sugar through photosynthesis..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Type 2 diabetes mellitus often leads to muscle atrophy driven by diminished differentiation capacity in myoblasts. Myogenesis is complex, and while many involved pathways have been described, there may still be yet undiscovered therapeutic targets. With this goal in mind, a recent study combined experiments in diabetic mice and cultured myoblasts to identify key proteins in diabetes-induced atrophy. The gene for the relatively undescribed solute carrier Slc2a6, also known as glut6, was up-regulated during myogenic differentiation and down-regulated during diabetes-induced myopathy. Silencing Slc2a6 with RNAi in cell culture impaired differentiation and myotube formation. Transcriptomics and metabolomics revealed that Slc2a6 silencing disproportionally impacted the glycolysis pathway . Further experiments and analysis determined that Slc2a6 regulates myogenic differentiation in cultured myoblasts and that this regulation was partly through the glycolysis pathway..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Patients with osteoarthritis typically experience progressive cartilage degeneration, joint inflammation, and bony growth around the joints. Treatment of this painful condition remains difficult because the underlying mechanisms aren’t clear, but recent evidence suggests that an increase in aerobic glycolysis, a form of glucose metabolism, may play a role. Aerobic glycolysis is regulated in part by the enzyme hexokinase 2 (HK2), which is upregulated in the joint tissues of patients with osteoarthritis . In addition to participating in glycolysis, HK2 affects cell growth, proliferation, survival, organelle recycling, and death under the influences of various other osteoarthritis-related proteins and pathways. For example, HK2 activity is promoted by the PI3K/Akt pathway, which is activated in osteoarthritis cartilage and HK2 might activate the transcription factor NF-κB to encourage downstream inflammatory processes in joints..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Polycystic ovary syndrome (PCOS) is a common endocrine disease usually accompanied by infertility. In PCOS, granulosa cells (GCs) produce insufficient energy via glycolysis to support proper follicle (egg-releasing sac) development, resulting in a condition called follicular dysplasia. miRNAs in small vesicles (exosomes) within the follicular fluid can regulate GCs, but whether these miRNAs affect GC glycolysis in PCOS is unclear. To find out, a recent study sequenced the RNA in exosomes from clinical follicular fluid samples. Compared to controls, exosomes from patients with PCOS had higher levels of the miRNA miR-143-3p and lower levels of the miRNA miR-155-5p. Glycolysis pathways were also negatively regulated in PCOS exosomes. In vitro, experiments on a KGN cell PCOS model confirmed that miR-143-3p inhibited glycolysis by silencing the gene HK2. miR-155-5p normally blocks miR-143-3p’s activity, so the miR-155-5p downregulation in PCOS permitted miR-143-3p to silence HK2..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.