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Publications by Sandra Kunder

Mutation of All Runx (AML1/Core) Sites in the Enhancer of T-Lymphomagenic SL3-3 Murine Leukemia Virus Unmasks a Significant Potential for Myeloid Leukemia Induction and Favors Enhancer Evolution Toward Induction of Other Disease Patterns

Journal of Virology

English

Impairment of Alternative Splice Sites Defining a Novel Gammaretroviral Exon Within Gag Modifies the Oncogenic Properties of Akv Murine Leukemia Virus

English

Related publications

Stability of AML1 (Core) Site Enhancer Mutations in T Lymphomas Induced by Attenuated SL3-3 Murine Leukemia Virus Mutants.

English

Increased Induction of Osteopetrosis, but Unaltered Lymphomagenicity, by Murine Leukemia Virus SL3-3 After Mutation of a Nuclear Factor 1 Site in the Enhancer

English

Increased Lymphomagenicity and Restored Disease Specificity of AML1 Site (Core) Mutant SL3-3 Murine Leukemia Virus by a Second-Site Enhancer Variant Evolved in Vivo.

English

Second-Site Proviral Enhancer Alterations in Lymphomas Induced by Enhancer Mutants of SL3-3 Murine Leukemia Virus: Negative Effect of Nuclear Factor 1 Binding Site.

English

AML1 (Acute Myeloid Leukemia 1)

Atlas of Genetics and Cytogenetics in Oncology and Haematology

English

The E47 Transcription Factor Binds to the Enhancer Sequences of Recombinant Murine Leukemia Viruses and Influences Enhancer Function.

English

CCAAT/Enhancer Binding Proteins Repress the Leukemic Phenotype of Acute Myeloid Leukemia

English

Induced Expression From the Moloney Murine Leukemia Virus Long Terminal Repeat During Differentiation of Human Myeloid Cells Is Mediated Through Its Transcriptional Enhancer.

Molecular and Cellular Biology

Cell Biology

Molecular Biology

1989

English

Tissue Distribution and Timing of Appearance of Polytropic Envelope Recombinants During Infection With SL3-3 Murine Leukemia Virus or Its Weakly Pathogenic SL3 Myb5 Mutant

English

Amanote Research

Discover open access scientific publications

Search, annotate, share and cite publications

Publications by Sandra Kunder

Mutation of All Runx (AML1/Core) Sites in the Enhancer of T-Lymphomagenic SL3-3 Murine Leukemia Virus Unmasks a Significant Potential for Myeloid Leukemia Induction and Favors Enhancer Evolution Toward Induction of Other Disease Patterns

Impairment of Alternative Splice Sites Defining a Novel Gammaretroviral Exon Within Gag Modifies the Oncogenic Properties of Akv Murine Leukemia Virus

Related publications

Stability of AML1 (Core) Site Enhancer Mutations in T Lymphomas Induced by Attenuated SL3-3 Murine Leukemia Virus Mutants.

Increased Induction of Osteopetrosis, but Unaltered Lymphomagenicity, by Murine Leukemia Virus SL3-3 After Mutation of a Nuclear Factor 1 Site in the Enhancer

Increased Lymphomagenicity and Restored Disease Specificity of AML1 Site (Core) Mutant SL3-3 Murine Leukemia Virus by a Second-Site Enhancer Variant Evolved in Vivo.

Second-Site Proviral Enhancer Alterations in Lymphomas Induced by Enhancer Mutants of SL3-3 Murine Leukemia Virus: Negative Effect of Nuclear Factor 1 Binding Site.

AML1 (Acute Myeloid Leukemia 1)

The E47 Transcription Factor Binds to the Enhancer Sequences of Recombinant Murine Leukemia Viruses and Influences Enhancer Function.

CCAAT/Enhancer Binding Proteins Repress the Leukemic Phenotype of Acute Myeloid Leukemia

Induced Expression From the Moloney Murine Leukemia Virus Long Terminal Repeat During Differentiation of Human Myeloid Cells Is Mediated Through Its Transcriptional Enhancer.

Tissue Distribution and Timing of Appearance of Polytropic Envelope Recombinants During Infection With SL3-3 Murine Leukemia Virus or Its Weakly Pathogenic SL3 Myb5 Mutant