K-ras Gene
K-ras Gene - Related Videos
02:38
The Ras Gene
0 Views •
2021
The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis. Ras is a superfamily...
02:38
The Ras Gene
0 Views •
2023
The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis. Ras is a superfamily...
01:24
Small GTPases - Ras and Rho
0 Views •
2023
Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides. Three regulatory proteins control their activity: Guanine nucleotide exchange factors or GEF, GTPase-activating proteins or GAPs, and Guanine nucleotide-dissociation inhibitors or GDIs. The GEF activates the GTPase by exchanging the bound-GDP with GTP. The GTPases’...
08:12
Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans
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Cited by 4 •
2020
The genetically tractable nematode Caenorhabditis elegans can be used as a simple and inexpensive model for drug discovery. Described here is a protocol to identify anticancer therapeutics that inhibit the downstream signaling of RAS and EGFR proteins.
12:55
Using the Gene Pulser MXcell Electroporation System to Transfect Primary Cells with High Efficiency
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Cited by 11 •
2010
This procedure shows how to use the Gene Pulser MXcell electroporation system to rapidly and easily identify the best electroporation conditions for mouse embryonic fibroblasts (MEFs) or other primary cells. Considerations for troubleshooting are also discussed in the associated video.
FAQs
Mutations in K-ras can disrupt the normal balance between its GTP-bound and GDP-bound forms. When the altered protein remains predominantly GTP-bound, signaling is no longer appropriately limited, allowing downstream growth and survival programs to remain active. This mechanistic shift explains why particular variants are investigated as potential drivers of abnormal cell proliferation and tumor development.
They are major downstream signaling routes through which altered K-ras activity can influence cell behavior. Persistent signaling through RAF-MEK-ERK or PI3K-AKT connects the molecular change to outcomes such as proliferation and survival, while pathway analysis helps researchers determine how a variant affects cellular regulation rather than treating the mutation as an isolated genetic event.
In normal biology, K-ras signaling participates in regulated control of proliferation, differentiation, and survival. Disease-associated mutations are concerning because they can favor the active state and produce persistent downstream signaling, unlike a cycle that more effectively alternates between active and inactive forms. This distinction helps explain how one altered signaling component can influence broader cellular behavior.
K-ras analysis can identify oncogenic variants and support tumor classification. Those results may inform treatment selection by distinguishing tumors according to their molecular features, and they also provide a basis for evaluating targeted inhibitors. Thus, the analysis links genetic findings with both diagnostic interpretation and the design or assessment of treatment strategies in cancer studies.
Researchers evaluate targeted inhibitors in the context of tumors carrying relevant K-ras alterations, using the analysis to connect a molecular variant with treatment strategy. Experimental models extend this work by showing whether altered signaling remains associated with tumor development or therapeutic resistance. Together, these approaches support assessment of inhibitor activity and the biological consequences of pathway alteration.
A variant identifies a molecular change, but an experimental model can clarify its functional consequences. Such models can show how altered signaling contributes to tumor development and therapeutic resistance, questions that variant identification alone cannot resolve. In Biology, this distinction is important because it connects a molecular observation to behavior in a tumor system and helps researchers test targeted inhibitors in a defined experimental context.