Related Experiment Video

Updated: Aug 19, 2026

Merging Absolute and Relative Quantitative PCR Data to Quantify STAT3 Splice Variant Transcripts
11:19

Merging Absolute and Relative Quantitative PCR Data to Quantify STAT3 Splice Variant Transcripts

Published on: October 9, 2016

Requirement for a signal sequence in biological expression of the v-sis oncogene

M Hannink, D J Donoghue

    Science (New York, N.Y.)
    |December 7, 1984
    PubMed

    Insights

    The simian sarcoma virus oncogene (v-sis) protein requires a specific signal sequence for its transforming activity. Mutating or removing this sequence, or altering it via point mutation, abolishes this biological function.

    Area of Science:

    • Oncogenic viral proteins
    • Retroviral gene function
    • Molecular biology of transformation

    Background:

    • The simian sarcoma virus oncogene (v-sis) encodes a protein implicated in cellular transformation.
    • Understanding the functional domains of viral oncogenes is crucial for deciphering oncogenesis.

    Purpose of the Study:

    • To investigate the role of the signal sequence in the biological activity of the v-sis protein.
    • To determine the necessity of the signal sequence for viral transformation.

    Main Methods:

    • Deletion mutagenesis to remove the signal sequence.
    • Fusion of inactive mutants with heterologous signal sequences.
    • Site-directed mutagenesis to introduce point mutations within the signal sequence.

    Main Results:

    • Removal of the v-sis signal sequence correlated with a loss of transforming activity.
    • Restoration of activity in deletion mutants upon fusion with a heterologous signal sequence.
    • Specific deletions or point mutations within the signal sequence abolished biological activity.

    Conclusions:

    • The signal sequence is essential for the transforming activity of the v-sis protein.
    • The integrity of the signal sequence is critical for its function in viral oncogenesis.

    More Related Videos

    Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo12:42

    Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo

    Published on: January 7, 2019

    Determining the Likelihood of Variant Pathogenicity Using Amino Acid-level Signal-to-Noise Analysis of Genetic Variation07:15

    Determining the Likelihood of Variant Pathogenicity Using Amino Acid-level Signal-to-Noise Analysis of Genetic Variation

    Published on: January 16, 2019

    Related Concept Videos

    Cis-regulatory Sequences02:02

    Cis-regulatory Sequences

    Cis-regulatory sequences are short fragments of non-coding DNA that are present on the same chromosomes as the genes that they regulate. These fragments serve as binding sites for transcriptional regulators, proteins that are responsible for controlling gene transcription and differential gene expression across cell types in eukaryotes. Cis-regulatory sequences can be close to the gene of interest or thousands of bases away in the DNA sequence; however, those sequences that are further away are...
    Cancer-Critical Genes II: Tumor Suppressor Genes01:05

    Cancer-Critical Genes II: Tumor Suppressor Genes

    Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
    When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
    Such genes that act...
    Rous Sarcoma Virus (RSV) and Cancer01:03

    Rous Sarcoma Virus (RSV) and Cancer

    Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
    RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
    Cis-regulatory Sequences02:02

    Cis-regulatory Sequences

    Cis-regulatory sequences are short fragments of non-coding DNA that are present on the same chromosomes as the genes that they regulate. These fragments serve as binding sites for transcriptional regulators, proteins that are responsible for controlling gene transcription and differential gene expression across cell types in eukaryotes. Cis-regulatory sequences can be close to the gene of interest or thousands of bases away in the DNA sequence; however, those sequences that are further away are...
    Cancer-Critical Genes II: Tumor Suppressor Genes01:05

    Cancer-Critical Genes II: Tumor Suppressor Genes

    Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
    When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
    Such genes that act...
    Rous Sarcoma Virus (RSV) and Cancer01:03

    Rous Sarcoma Virus (RSV) and Cancer

    Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
    RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...