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:

"Gq protein-coupled receptors (GqPCRs) are membrane bound proteins that transmit signals from outside the cell to internal signaling pathways. One of these pathways is the PI3K/AKT pathway, which plays roles in cellular proliferation, survival, metabolism, and differentiation. PI3K/AKT dysregulation is also often implicated in cancers. A previous study determined that activating GqPCRs in certain cells inactivated AKT, which led to a specific type of cell death, JNK-dependent apoptosis. This unique signal seems to play an important role in physiological and pathological events like pituitary development and cardiac hypertrophy. Now, a new study determined that the mechanism of this AKT inactivation relies on another signaling-related protein, PP2A. When the GqPCRs are not activated, a fraction of PP2A "c" subunit is in a dimer complex with another protein, IGBP1 and they are bound to the p85 subunit of PI3K, causing its activation..."

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:

"Apoptosis is a form of cell death that occurs as part of normal development. Once considered irreversible, apoptosis might not mark the end for all cells—including cancer cells. Growing evidence suggests that cancer cells can be rescued from the brink of death through a process called anastasis, which could explain how tumors resist anticancer therapies. From the Greek for “resurrection,” anastasis can occur through a variety of mechanisms, such as by arresting the activity of caspases, enzymes in charge of dismantling the cell during apoptosis by activating DNA repair mechanisms and by allowing cell fragments to fuse and continue living even after apoptosis has begun. Further studies are needed to explore how cancer cells cheat death through anastasis and how to adjust anticancer therapies accordingly..."

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

How apoptosis is different from cell death by injury. Role in development and body maintenance.

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:

"Parasitic infections affect nearly 1 in 6 people worldwide. These infections thrive when parasites are able to evade, inhibit, or disrupt host defense mechanisms. One way parasites avoid the immune response is to disguise themselves as dying host cells. Normal host cells undergoing apoptosis expose a molecule called phosphatidylserine (PS) on the plasma membrane as a signal to surrounding cells. This signal is detected by phagocytic immune cells, which engulf the dying cell and reduce inflammation. The system is co-opted by parasites, who use PS as a Trojan horse to enter phagocytic immune cells, infecting the host. This process, known as “apoptotic mimicry, ”takes several forms. Classical apoptotic mimicry - where the PS comes from the challenger - is used by the parasites that cause leishmaniasis, American trypanosomiasis, and toxoplasmosis; while non-classical apoptotic mimicry, which co-opts PS exposed by dying host cells, is used by the parasites that cause malaria and amebiasis..."

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

Biology is designed for multi-semester biology courses for science majors. It is grounded on an evolutionary basis and includes exciting features that highlight careers in the biological sciences and everyday applications of the concepts at hand. To meet the needs of today’s instructors and students, some content has been strategically condensed while maintaining the overall scope and coverage of traditional texts for this course. Instructors can customize the book, adapting it to the approach that works best in their classroom. Biology also includes an innovative art program that incorporates critical thinking and clicker questions to help students understand—and apply—key concepts.

By the end of this section, you will be able to:Describe how signaling pathways direct protein expression, cellular metabolism, and cell growthIdentify the function of PKC in signal transduction pathwaysRecognize the role of apoptosis in the development and maintenance of a healthy organism

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:

"Leukemia relapse after conventional treatments is difficult to treat and has high patient mortality. Relapse is driven by the reawakening of previously quiescent cancer cells. Traditional treatments are ineffective against quiescent cells, as they instead target rapidly dividing cells. A new study investigated a potential dual-target treatment, C212, in cell culture. C212 is a derivative of curcumin, a compound that has shown anticancer properties in previous research. C212 was effective against both growing and quiescent leukemia cells. C212 drives quiescent leukemia cells deeper into dormancy by increasing their exit threshold, and then kills these deep-quiescent cells. This differs from previous strategies that awaken quiescent cells to kill, which runs the risk of wakening treatment-resistant subpopulation of cells. Molecular docking and experimental analyses showed that C212 could bind to Hsp90 and interferes with its function..."

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:

"Apoptosis, a form of programmed cell death, plays critical roles in animal development and in repair of DNA damage. Since DNA damage is a major factor in cancer development, identifying the regulators of damage-induced apoptosis could help researchers develop treatments. A recent study investigated whether NHR-14, an important developmental protein in the model organism C. elegans, also contributes to damage-induced apoptosis . using mutant C. elegans that are especially susceptible to radiation-induced DNA damage. Deletion of the gene encoding NHR-14, which corresponds to HNF4 in humans, decreased radiation-induced apoptosis of sex cells without affecting the levels of normal (non-damage-induced) apoptosis, indicating a specific role in the damage-induced death pathway. Further exploration revealed that the NHR-14 gene acts “downstream” of the DNA damage checkpoint pathway and regulates the transcription of the genes egl-1 and ced-13 after DNA is damaged..."

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:

"Thrombospondin-1, or TSP-1, is a calcium-binding protein implicated in the development of several diseases, including diabetes, cancer, renal failure, and cardiovascular disease. To understand TSP-1’s role in disease, researchers recently examined the protein’s effects on the calcium dynamics, survival, and deformability of red blood cells. In vitro experiments showed that exposure to recombinant human TSP-1 significantly increased calcium levels in red blood cells. TSP-1 treatment also induced an inward ionic current, suggesting possible calcium influx through non-selective cation channels, and TSP-1 caused the deformation of red blood cells. Further experiments revealed that TSP-1 binding to its receptor CD47 could dictate the lifespan of red blood cells in circulation. Altogether, the findings suggest that TSP-1/CD47 signaling could be one targetable pathway in systemic diseases that attack red blood 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:

"Glioblastoma is a devastatingly aggressive and prevalent primary brain tumor. Despite the discovery of many potential biomarkers and treatment targets, there has been little improvement in survival. One unexplored pathway in glioblastoma is chaperone-mediated autophagy (CMA), which has been implicated in a variety of human malignancies. A new paper examined CMA and its key component, lysosome-associated membrane protein type 2A (LAMP-2A), using clinical samples, in vitro experiments, and a mouse xenograft model. In clinical samples, glioblastoma showed elevated expression of LAMP-2A compared to peritumoral regions and low-grade glioma and an associated decrease in nuclear receptor co-repressor (N-CoR). Glioblastoma with high LAMP-2A expression also had inhibited unfolded protein response and apoptosis. In vitro, silencing LAMP-2A up-regulated N-CoR and activated the unfolded protein response pathway, which led to apoptosis..."

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:

"Diabetic kidney disease is one of the major causes of death in patients with diabetes and the leading cause of end-stage renal disease in the United States. One early sign believed to contribute to diabetic kidney disease is injury to the glomerulus. The glomerulus is a cluster of blood vessels in the kidney that filters excess fluid and waste products out of the blood. However, the molecular mechanisms that lead to irreversible glomerular injury in the setting of diabetes are poorly understood. To gain a clearer picture, researchers evaluated the impact of the diabetic microenvironment on glomerular endothelial cells. Prolonged exposure to diabetic serum affected mitochondria. resulting in cellular dysfunction, but not cell death..."

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:

"FAF1 is a protein involved in various biochemical processes including cell death, inflammation, and cell proliferation and is implicated in certain diseases, including cancer and Parkinson’s disease. To date, FAF1 has been assumed to be locked within the cytosol—with no secretion mechanism reported for the protein. Now, researchers have discovered two mechanisms by which FAF1 can be secreted and transmitted between cells. Experiments on human neuroblastoma cells showed that FAF1 was secreted as cargo within exosomes, as well as in a free, non-exosomal form. Experiments also showed that FAF1 promoted the formation of exosomes, suggesting a regulatory role for the protein in exosome biogenesis. Additionally, extracellular FAF1 was transmitted to neighboring neuronal cells via endocytosis, triggering cell death through apoptotic and necrotic pathways. As the first to reveal these FAF1 secretion pathways this study could lead to ways of interfering with cell death by inhibiting FAF1 secretion..."

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:

"p53 is widely considered the most frequently mutated gene in human disease, including in cancer. Normally, p53 acts as a checkpoint for recognizing DNA damage and actually suppresses tumor formation. Alterations to p53 compromise this function and can make way for life-threatening tumor growth. A new study examined how abnormal p53 might create conditions favorable for one of the most aggressive forms of ovarian carcinoma. The authors of the study began by knocking the p53 gene out of ovarian carcinoma cells and monitoring the effects. Next-generation sequencing of the p53-less cells revealed significantly elevated expression of fibronectin, a structural protein linked to various carcinomas. Loss of p53 function also appeared to boost the cancer cells’ ability to migrate and spread. Data on actual patients with ovarian cancer confirmed the pattern observed in the lab..."

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:

"Gallbladder cancer (GBC) is becoming increasingly common, especially in American Indian and Southeast Asian populations. Early GBC can be successfully removed with surgery, but advanced GBC has a poor prognosis . and the existing treatments have many side effects. To explore better therapies, researchers recently investigated the anti-GBC effects of penfluridol, an antipsychotic drug with anticancer activity. In vitro, penfluridol (PF) strongly inhibited the replication and invasion of three GBC cell lines, confirming its anti-GBC potential, but it also dramatically increased glucose consumption via glycolysis, which is a hallmark of cancer. Specifically, penfluridol activated the AMPK/PFKFB3 glycolysis pathway. However, inhibiting glycolysis, particularly the AMPK/PFKFB3 pathway (with Compound C, CC) solved this problem enhancing penfluridol’s GBC-killing effects. The same synergistic effects were observed in mouse tumor models in vivo..."

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:

"Researchers are combining tumor-killing viruses with immune-boosting drugs to mark otherwise stealthy tumors for death In their recent study, the researchers grafted human melanoma tumors onto the left and right flanks of mice Right-side tumors were injected with ONCOS-102, viruses genetically modified to eradicate melanoma cells Left-side tumors were left untreated The team then injected mice with pembrolizumab, a checkpoint inhibitor Checkpoint inhibitors block cloaking proteins on tumor or T cells that normally let them slip past immune cells These powerful drugs turn “cold” tumors “hot” on immune cells’ radar Shrunken left-side tumors proved that this 1-2 combination could cripple tumors at a distance— an effect amplified by delivering ONCOS-102 and pembrolizumab at the same time Now, in order to prove the efficacy of ONCOS-102 combined with pembrolizumab in humans, a Phase I clinical study is ongoing (NCT03003676) Researchers are exploring how to make this killer combi.."

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 diabetic nephropathy (DN), a common complication of diabetes, the structure and function of the kidneys deteriorate. One early sign of DN is proteinuria, or protein excretion in urine. Although the mechanism of DN-related proteinuria isn’t clear, rearrangement of the cellular skeleton, or cytoskeleton, might contribute. A recent study explored this theory by examining the role of the cytoskeletal protein MAP4 in DN proteinuria. In urine from patients with diabetes as well as kidney tissues from diabetic mice, the content of phosphate-modified (phosphorylated) MAP4 was elevated. In mice, inducing MAP4 phosphorylation promoted the development of DN-like proteinuria with aging and caused podocytes, specialized kidney cells that prevent proteins from entering urine, to lose their epithelial characteristics and die. In addition, mice with induced MAP4 phosphorylation were much more susceptible to diabetes than normal mice..."

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:

"Synovitis is one of the most common and serious musculoskeletal diseases in horses, causing osteoarthritis and lameness. While available pharmaceutical treatments can reduce joint pain and inflammation, they are expensive and unable to prevent disease progression. Recently, researchers have started looking toward fibroblast-like synoviocytes (FLS) for the development of new treatment options. FLS are cells that produce lubricating proteins to protect cartilage from injury, But they lose their protective features and begin to produce inflammatory chemicals in horses with synovitis and ultimately cause the failure of the FLS mitochondrial machinery, cell death, and joint degeneration. A team of researchers thus transferred healthy mitochondria from immune cells into FLS to determine whether doing so could restore FLS function. They found decreases in cell proliferation and death after mitochondrial transfer as well as a reduction in the production of inflammatory proteins..."

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