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Source transformation is a fundamental technique employed in circuit analysis, offering a valuable tool for simplifying complex electrical circuits. This technique involves the replacement of either a voltage source in series with a resistor by a current source in parallel with a resistor, or vice versa. The key concept here is that when the original sources are deactivated (turned off), the equivalent resistance at the circuit's end terminals remains the same.
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Functional dissection of transformation by c-Src and v-Src.

Chitose Oneyama¹, Tomoya Hikita, Shigeyuki Nada

¹Department of Oncogene Research, Research Institute of Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.

Genes to Cells : Devoted to Molecular & Cellular Mechanisms

|January 5, 2008

Summary

Over-expressed c-Src (proto-oncogene) can transform cells, but requires a specific ratio with its regulator Csk. This transformation is distinct from v-Src, with limited downstream effects and slower tumor growth.

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Area of Science:

Oncology
Molecular Biology
Cell Biology

Background:

The c-src proto-oncogene is often over-expressed and activated in human cancers, suggesting its involvement in cancer progression.
Src family kinases, including c-Src, are regulated by negative regulators like Csk (C-terminal Src kinase).

Purpose of the Study:

To investigate the transforming potential of c-Src in mouse embryonic fibroblasts lacking Csk.
To determine the threshold for c-Src-induced transformation based on the c-Src:Csk ratio.
To compare the transforming mechanisms and downstream effects of c-Src with those of v-Src.

Main Methods:

Analysis of cell transformation phenotypes (anchorage-independent growth, tumorigenicity) in Csk-deficient mouse embryonic fibroblasts with c-Src over-expression.
Dose-dependent inhibition studies by re-expressing Csk.
Comparison of protein phosphorylation profiles and gene expression changes induced by c-Src versus v-Src.
In vivo tumor growth and angiogenesis assessment.

Main Results:

c-Src over-expression induced transformed phenotypes in Csk-deficient cells, with transformation being dependent on the c-Src:Csk ratio.
c-Src induced limited protein phosphorylation and gene expression changes compared to v-Src.
Key v-Src targets like STAT3 were not significantly activated by c-Src.
Genes such as cyclin D1 and HIF-1alpha, involved in cancer progression, were induced by v-Src but not c-Src.
c-Src tumors exhibited slower growth and hematoma formation, contrasting with v-Src tumors' aggressive growth and angiogenesis.

Conclusions:

c-Src possesses cell transformation potential, but its oncogenic activity is modulated by the c-Src:Csk ratio.
c-Src-induced transformation is distinct from v-Src, with a more restricted molecular and cellular impact.
Additional pathways are likely required for c-Src to fully promote tumor progression in vivo.