Hras Nras Kras
Hras Nras Kras - Related Videos
02:36
Establishing a Murine Tumor Cell Line In Vitro Using a Virus-Cas9 System
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2026
Source: Prasad, M. et al. In Vitro Establishment of a Genetically Engineered Murine Head and Neck Cancer Cell Line using an Adeno-Associated Virus-Cas9 System. J. Vis. Exp. (2020)This video demonstrates the in vitro transformation of murine epithelial cells through viral delivery of Cre recombinase and mutation-inducing components. It outlines the steps for Cas9 activation, cancer-gene modification, and the establishment of a tumorigenic murine cell line.
08:24
Nitrogen Cavitation and Differential Centrifugation Allows for Monitoring the Distribution of Peripheral Membrane Proteins in Cultured Cells
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Cited by 15 •
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Here we present protocols for detergent-free homogenization of cultured mammalian cells based on nitrogen cavitation and subsequent separation of cytosolic and membrane-bound proteins by ultracentrifugation. This method is ideal for monitoring the partitioning of peripheral membrane proteins between soluble and membrane fractions.
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Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma
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Cited by 44 •
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Here we describe an efficient and versatile protocol to induce, monitor and analyze novel glioblastomas (GBM) using transposon DNA injected into the ventricles of neonatal mice. Cells of the subventricular zone, which take up the plasmid, transform, proliferate and generate tumors with histo-pathological characteristics of human GBM.
10:13
A Multiplexed Luciferase-based Screening Platform for Interrogating Cancer-associated Signal Transduction in Cultured Cells
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Cited by 6 •
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Achieving a systems level understanding of cellular processes is a goal of modern-day cell biology. We describe here strategies for multiplexing luciferase reporters of various cellular function end-points to interrogate gene function using genome-scale RNAi libraries.
09:18
Multianimal Magnetic Resonance Imaging for Tumor Measurements in Pancreatic Cancer Mouse Models
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2026
This protocol uses a multichamber bed for parallel magnetic resonance imaging (MRI) of up to four animals to detect pancreatic adenocarcinoma tumors in genetically engineered mouse models. This multianimal MRI protocol is fast and cost-effective for detecting and measuring tumors, facilitating animal selection for preclinical studies and longitudinal monitoring of tumor growth.
FAQs
Ras signaling is controlled by the balance between nucleotide exchange and GTP hydrolysis. Signals from cell-surface receptors promote replacement of GDP with GTP, switching the protein into its active state. Intrinsic hydrolysis, assisted by other factors, converts GTP back toward the inactive GDP-bound state, allowing signal duration to be regulated rather than continuously maintained.
Mutations that impair the normal exchange and hydrolysis cycle can leave Ras proteins in their active state for extended periods. Instead of responding transiently to regulated cellular signals, the affected pathway can continue promoting processes such as cell growth and survival. This persistent activity provides a mechanistic link between altered Ras genes and abnormal proliferation.
HRAS, NRAS, and KRAS encode closely related Ras small GTPase proteins, so studying them together reveals shared principles of regulated cellular signaling. Their combined study supports analysis of growth, survival, differentiation, and related processes while also allowing researchers to examine how disruption of a common molecular switching system contributes to disease biology.
The nucleotide-bound state determines whether Ras signaling is inactive or active. GDP binding corresponds to the restrained state, whereas receptor-stimulated exchange produces the GTP-bound form that transmits growth-related signals. Returning toward GDP through hydrolysis helps terminate that activity, making the transition important for coordinating cellular responses with changing external signals.
Analysis of HRAS, NRAS, and KRAS connects molecular signaling with both normal and abnormal biology. Because Ras proteins regulate growth, survival, and differentiation, their study helps explain developmental pathways. The same framework clarifies how disrupted signaling contributes to cancer biology, linking gene-level changes with altered cellular behavior and proliferation.
Ras gene analysis can contribute to the classification of tumors by identifying changes in a signaling system strongly associated with abnormal proliferation. Examining these genes places tumor biology in a molecular context rather than relying only on general growth characteristics. This information can support comparisons among tumors and help organize disease-related patterns.
These genes are relevant to targeted therapy efforts because mutations that maintain Ras proteins in an active state can drive disease-associated signaling. Understanding the nucleotide cycle and its disruption provides a mechanistic basis for seeking interventions directed at Ras-driven disease. The research goal is to connect molecular abnormalities with more focused therapeutic strategies.
Ras-related findings should be interpreted in relation to several connected outcomes, including cell growth, survival, and differentiation. A change in the signaling cycle may therefore have consequences beyond proliferation alone. Considering these processes together helps researchers evaluate developmental effects, understand cancer-associated behavior, and relate molecular observations to broader biological functions.