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:

"Metabolic syndrome refers to dysregulated metabolism that’s associated with increased risks of diabetes, heart disease, and stroke. In women, this syndrome becomes more in common after menopause, when levels of circulating 17β-estradiol drop. Estrogen replacement therapy can help, but its long-term use is linked to other problems, like gynecological cancers. To explore new options, researchers recently administered butyrate, a fatty acid, to mice with metabolic syndrome whose ovaries had been removed, as butyrate has been shown to alleviate obesity and insulin resistance, both of which are linked to metabolic syndrome. The researchers found that oral butyrate reduced body fat and blood lipid levels in the mice while increasing whole-body energy usage and improving insulin sensitivity. Investigation of the mechanism in cultured muscle cells revealed that butyrate induced expression of the estrogen receptor ERα and activated the proteins AMPK and PGC1α..."

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:

"Bone morphogenetic proteins (BMPs) regulate cell-fate decisions during embryonic development. But after birth, dysfunctional BMP expression is linked to some human diseases, like carcinomas. In lung cancer, BMPs are reactivated and suppress AMPK signaling. Mitochondrial stress activates AMPK to a ‘normal’ level, where it promotes cancer cell survival, but AMPK can induce cell death if ‘hyperactivated.' BMPs inhibit LKB1, a kinase that can hyperactivate AMPK, making BMPs a potential therapeutic target. So, researchers tested two BMP inhibitors as a combination treatment with mitochondrial targeting agents. In lung cancer cell lines that express LKB1, the combination treatment activated AMPK and suppressed cell growth. The combination treatment was increasing nuclear localization of the aptly named apoptosis inducing factor (AIF) in these cells, an effect that depended on LKB1 expression..."

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:

"In lactating mammals, the mammary glands are responsible for milk production and secretion. Low energy levels in mammary gland cells are known to reduce milk synthesis by activating AMPK, an energy-sensing protein. However, the exact mechanism by which energy status affects lactation efficiency isn’t clear. To learn more, researchers recently examined AMPK’s role in milk synthesis in mouse mammary epithelial cells. Energy (glucose) deficiency indeed activated AMPK, which reduced milk fat and protein synthesis in the cells. AMPK inhibited milk production partly by inhibiting the classic mTORC1 signaling pathway, but it primarily reduced milk protein synthesis by blocking the signaling pathway of the lactation hormone prolactin. Specifically, AMPK triggered degradation of the prolactin receptor (PrlR) in lysosomes to halt prolactin signaling..."

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:

"For over 1,000 years, the extract from Magnolia tree bark has been a popular elixir, treating everything from anxiety to muscle pain. Now, researchers have discovered how Magnolia extract might help treat oral cancer. In mice with oral tumors, the extract suppressed the growth and spread of cancer cells. Experiments revealed three key active compounds responsible for this preventive effect: honokiol, magnolol, and 4-O-methylhonokiol, which are found in many traditional herbal medicines. These compounds acted like poison against oral cancer cells, crippling their ability to fend off harmful oxidants. Understanding how or whether this same mechanism occurs in humans will be crucial, as it could help clarify how Magnolia extract fights cancer and other disorders..."

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:

"Heart disease is the leading cause of death worldwide. While people have benefited greatly from advances in drugs and surgery, one glaring problem remains: unlike the cells that make up our other muscles, once heart cells are gone, they simply can’t be regenerated. That is, unless you were just born. Studies show that muscle cells in the hearts of newborn mice, rabbits, and even humans can go on dividing for up to days after birth. And now, in what could be a new world record, scientists have recorded signs of regeneration beyond two weeks after birth in the South American gray short-tailed opossum. Their ability to replicate this feat in mice could point to new ways of healing the hearts of humans with cardiovascular disease. The experiments that led to these results were carried out by Wataru Kimura and colleagues at the RIKEN Center for Biosystems Dynamics Research in Japan..."

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:

"Oncogenic PIM kinases and the tumor suppressor LKB1 regulate cell growth and metabolism in different directions. LKB1 suppresses tumorigenesis largely by phosphorylating and activating the energy sensing kinase AMPK. Anti-oncogenic PIM inhibitors also increase AMPK phosphorylation. However, the exact mechanism by which PIM inhibition affects AMPK remains unclear. A recent study explored the potential PIM-LKB1 interaction related to AMPK phosphorylation in prostate (PC3) and breast (MCF7) cancer cells. Inhibition of activity (by DHPCC9 or AZD1208) or expression (by triple knockout, TKO) of all three PIM kinases increases AMPK phosphorylation. These effects are LKB1-dependent, suggesting that PIM kinases regulate AMPK via LKB1. Additional assays confirmed that PIM kinases phosphorylate LKB1 to inactivate it, identifying LKB1 as a novel PIM substrate. In a chick embryo xenograft model, LKB1 knockout increased tumorigenic growth of prostate cancer cells..."

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:

"One hallmark of neurodegenerative diseases such as Alzheimer's and Parkinson's is protein accumulation in the brain. That accumulation is driven by structural modification of the cellular prion protein. which produces self-generating particles in the brain. Neuronal cell death caused by these protein clusters occurs through autophagy, the body’s way of degrading damaged cells. Unfortunately, the pathways mediating prion-driven autophagy in neurons remain unclear. A recent study evaluated the role of calcium signaling – a common signaling pathway affected by prion proteins. Using neuronal cells from mice, researchers measured calcium signaling and the levels of proteins involved in metabolic stress and autophagy. Their results showed that human prion peptide increased the concentration of calcium in neurons. Inhibiting this prion-mediated calcium uptake in neurons prevented autophagic cell death. and preserved the activity of a protein called AMPK, which is involved in maintaining energy balance in cells..."

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:

"Antibody treatments such as cetuximab are powerful against colorectal cancer, but colorectal cancer cells are known to develop resistance to these drugs in large part due to to overactivation or mutation of the gene KRAS. To understand how KRAS might give rise to cetuximab resistance, researchers treated two types of lab-grown cells with the antibody, normal cancer cells and cancer cells containing a mutated KRAS gene. They then monitored the effects on AMPK, an enzyme that is toxic to various cancer cells. KRAS mutation impaired this AMPK-based defense, enabling mutant cancer cells to outlive normal cancer. Exposing cells with drugs known to activate AMPK, such as metformin, recovered the anti-cancer defense, overcoming the centuximab resistance induced by a mutated KRAS gene. That same mechanism was observed in colorectal tumors grafted onto mice. The results indicate that targeting AMPK could be a powerful therapeutic strategy, possibly boosting anti-cancer defenses in patients with colorectal cancer..."

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