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:

"Traumatic brain injury (TBI), or brain damage caused by a sudden blow or jolt to the head, is a leading cause of death and disability worldwide. The mechanisms are complex and differ among patients, making TBI difficult to treat, and anti-inflammatory agents that are effective in animal models have been less promising in human trials, indicating that better treatments are needed. To explore new strategies, a recent study investigated the effect of the anti-inflammatory compound ACT001 on TBI. In mice, ACT001 reduced brain damage and improved motor function after TBI by reducing trauma-induced activation of microglia, which are immune cells of the central nervous system. In vitro, ACT001 also reduced activation of mouse and rat microglia induced by the bacterial toxin lipopolysaccharide (LPS) and downregulated LPS-induced secretion of proinflammatory molecules in a mouse microglial cell line..."

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:

"Some proteins are central to many cell signaling processes. One of these key molecules is AKT2. An important kinase involved in cell survival, growth, and metabolism, it has ties to insulin-induced signaling and cancer. AKT2 has a critical role in immune cells such as neutrophils and macrophages; however, although AKT2 is expressed in antibody-producing immune cells called B cells, its function in B cells isn’t clear. In a recent study, researchers sought to understand the role of AKT2 in B cells using AKT2-deficient mice. They found that mice lacking AKT2 had impaired B-cell differentiation. B cells from these mice were not able to form a cluster of molecules called a signalosome in response to B-cell receptor (BCR) signaling, resulting in poor BCR signaling and impaired B cell activation and spreading. These results suggest that as a central orchestrator of signaling, AKT2 function is critical for proper BCR signaling and B cell development, ensuring a functional antibody-mediated immune response..."

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:

"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:

"In many cell types, growth factor stimulation triggers the formation of structures called circular dorsal ruffles (CDRs). CDRs are large, rounded ruffles on the upper cell membrane that serve as platforms for PI3K–PIP3–AKT protein signaling and probably play a role in cell growth. CDRs are present in some types of cancer cells, but it’s unclear whether they contribute to cancer development. To find out, researchers recently treated six cancer cell lines and one normal cell line with two growth factors: epidermal growth factor and insulin. Both growth factors induced CDR formation in the Hep3B hepatocellular carcinoma line, but not in normal liver cells, other hepatocellular carcinoma cells, breast cancer cells, or pancreatic cancer cells. Closer analysis confirmed that growth factor receptor proteins were recruited to the CDRs and that the PI3K–PIP3–AKT pathway was activated at the ruffles..."

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:

"The protein eIF6 is involved in ribosome formation and mRNA translation and is essential for the growth and reproduction of cells, including cancer cells. However, eIF6’s role in oral squamous cell carcinoma (OSCC) remains unclear. To learn more, researchers recently analyzed eIF6 in 233 OSCC samples and in OSCC cell lines. They found that cytoplasmic eIF6 expression was abnormally high in OSCC tissues and was associated with tumor size and clinical grade. Upregulating eIF6 promoted OSCC cell growth, migration, and invasion in vitro and enhanced tumor growth in vivo. eIF6 also encouraged epithelial-mesenchymal transition (EMT), a process necessary for cancer cell migration, in OSCC cells, but depletion of eIF6 (with sh-eIF6-2) suppressed the cancer-enhancing effects. Mechanistic studies revealed that eIF6 exerted its tumor progression-promoting effects by activating the AKT signaling pathway, and further experiments confirmed that eIF6 and AKT directly interacted in the cytoplasm..."

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:

"Glioblastomas are deadly, malignant brain tumors. Even with current treatment methods, the median life expectancy after diagnosis is only 15 months. This extreme treatment resistance is primarily due to changes in the tumor microenvironment (TME). Glioblastomas sometimes recruit normal cells to aid growth, and neural progenitor cells (NPCs) have been observed migrating toward glioblastomas. Understanding the interaction between tumor and non-tumor cells in the TME is critical to developing new treatments. Recently, researchers examined the effects of extracellular vesicles (EVs) from glioblastoma cell lines on the cell lines themselves and mouse NPCs (mNPCs). In both glioblastoma cell lines and mNPCs, glioblastoma-derived EVs promoted proliferation and migration. Using a combination of proteomic profiling and laboratory assays, researchers examined the potential mechanisms of this effect and identified the PI3K-Akt-mTOR pathway as a key mediator..."

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:

"Venous malformations are the most common vascular anomaly around the world. Extensive malformations cause pain, bleeding, anatomic distortion, and organ dysfunction. Current therapies are invasive and rarely curative, making it necessary to develop new treatment options. To that end, researchers examined one molecular mechanism known to lead to venous malformations, the interaction between endothelial and smooth muscle cells. The researchers screened 5 patients with the mutation known to cause venous malformations. Malformations with that mutation showed lower expression of platelet-derived growth factor beta and alpha-smooth muscle actin. In addition, mutant endothelial cells showed enhanced cell viability and motility, and decreased tube formation. These conditions could be reversed in vitro by rapamycin, which, experiments showed, worked by inhibiting the AKT-mTOR pathway. This pathway could therefore be an important target for disrupting the formation of venous malformations..."

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:

"Sialic acids are a family of sugars found throughout the body. They facilitate a variety of cellular functions such as interactions between cells and the detection of foreign bodies. But sialic acids are also linked to the progression of cancer, including bladder cancer. In a new study, researchers examined how bladder cancer cells rich in sialic acids respond to NEU1, one of several enzymes responsible for removing sialic acids from lipids and proteins. The team found that low NEU1 expression was linked to abnormally large amounts of sialic acids in cancer cells. In fact, low expression of NEU1 correlated with bladder cancer progression. High NEU1 expression, on the other hand, enhanced cancer cell death and decreased cancer proliferation. These findings were obtained for both cancer cells grown in the lab and cells extracted from mice with bladder cancer..."

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 individuals with Duchenne muscular dystrophy (DMD), lack of the protein dystrophin impairs autophagy and drastically disrupts myotube development. The PI3K/Akt/mTOR pathway is a vital autophagy-regulating pathway that also participates in skeletal muscle differentiation. However, the precise disruption of this pathway in the context of DMD remains unclear. To clarify the mechanism, researchers recently performed protein profiling on dystrophin-deficient myoblasts. The deficient (dfd13) myoblasts were not able to achieve terminal differentiation. They also exhibited strongly increased PTEN expression and perturbed PI3K/Akt/mTOR regulation. In addition, rictor-mTORC2 was inactivated, which caused FoxO3 misregulation and ultimately increased autophagy-related gene activation. Autophagosome formation was excessive in the dystrophin-deficient myoblasts; however, subsequent LC3B-I to LC3B-II conversion and autophagic flux were decreased, consistent with the known autophagy disruption in DMD..."

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:

"The protein IFNα can reduce growth and promote apoptosis of cancer cells by stimulating genes such as PML, whose deficiency is linked to tumorigenesis, but the contributions of different PML isoforms to the anticancer effects remain unclear. Given that PML-II positively regulates genes that are induced during the type I IFN response, researchers recently investigated whether and how PML-II participates in IFNα-induced cell death using a cervical cancer cell line. In cells with PML-II deletion (siPML-II), death during IFNα stimulation was reduced, and IFNα-induced ISG54 mRNA expression was attenuated. In addition, silencing PML-II decreased the expression of TRAIL and PUMA during IFNα stimulation, indicating that the extrinsic and intrinsic apoptosis pathways were blunted..."

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:

"Esophageal cancers are common globally but are difficult to treat and have a poor prognosis. Esophageal squamous cell carcinoma (ESCC) is especially dangerous and has poorly understood molecular mechanisms. A recent study took a comprehensive look at the kappa opioid receptor (KOR), a protein that has been shown to influence the progression of other cancers. First, researchers examined existing patient datasets and found that ESCC tumors had reduced KOR expression and that lower expression of KOR was correlated with reduced patient survival. In the lab, they found that reducing KOR expression in cultured ESCC cells led to increased proliferation, invasion, and metastasis. When looking for potential mechanisms, they found that down-regulation of KOR activated the PDK1-AKT signaling pathway. It also led to invasion-related changes in cells, including invadopodia formation and cytoskeletal rearrangement. Reducing expression of KOR in mice led to increased metastasis and phosphorylation of the AKT enzyme..."

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:

"The Slit/Robo signaling molecules are famous for controlling how the axons of neurons reach their targets. But the proteins also have other functions, including a newly discovered role in the testes. Researchers at the University of Montreal studied Slit/Robo in the adult mouse testis. The team found the molecules expressed in the tissue, particularly in Leydig cells. These cells produce testosterone in response to luteinizing hormone. When treated with SLIT ligands, cultured Leydig cells reduced their expression of various steroidogenic genes. SLIT2 treatment also drove down the expression of a receptor. This diminished the ability of a Leydig cell line to respond to luteinizing hormone. On the flip side, mice without Robo1 had higher levels of intra-testicular testosterone. And Slit and Robo expression was augmented by in vitro testosterone treatment..."

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:

"Triple-negative breast cancer (TNBC) is a highly aggressive form of breast cancer with a poor prognosis and limited treatment options. M2-like tumor-associated macrophages (TAMs) are known to promote TNBC aggressiveness, but the mechanisms are unclear. To learn more, a recent study investigated the roles of TAMs in regulating epithelial–mesenchymal transition (EMT) and cancer stem cell (CSC) properties in TNBC, both of which contribute to malignant progression. The results revealed that human TNBC tissues exhibited severe infiltration of TAMs (marked by CD163) and that TAMs were associated with an unfavorable prognosis. In addition, culture media from TAM-like macrophages promoted EMT and CSC-like properties in two TNBC cell lines. Specifically, TAM-secreted CCL2 protein activated AKT signaling to increase β-catenin expression and nuclear localization, and knockdown experiments confirmed the importance of β-catenin in the TAM-induced changes..."

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:

"Autophagy is an essential intracellular recycling and degradation process. Dysfunction of autophagy is associated with diseases such as cancer, neurodegeneration, and cardiovascular disease. Some of these diseases don’t have effective treatments, underscoring the need for a thorough understanding of autophagy regulation. The protein complexes mTORC1 and mTORC2 are both autophagy regulators. mTORC1’s inhibitory effect on autophagy is well described, but mTORC2’s role is more complex and less understood. For example, mTORC2 can suppress autophagy by activating the proteins AKT and SGK-1. For example, mTORC2 can suppress autophagy by activating the proteins AKT and SGK-1, but promote autophagy by activating the protein PKCα. The activity of mTORC2 itself can also be modulated by upstream factors such as nutrients and intracellular signals and through positive and negative feedback mechanisms involving insulin, mTORC1, and other molecules..."

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