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accession-icon GSE32277
Kras is required for pancreatic tumor maintenance through regulation of hexosamine biosynthesis and the non-oxidative pentose phosphate pathway
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon

Description

The maintenance of advanced malignancies relies on continued activity of driver oncogenes, although their rate-limiting role is highly context-dependent with respect to tumor types and associated genetic alterations. Oncogenic Kras mutation is the signature event in human pancreatic ductal adenocarcinoma (PDAC), serving a critical role in tumor initiation. Here, an inducible KrasG12D-driven p53 mutant PDAC mouse model establishes that advanced PDAC remains strictly dependent on continued KrasG12D expression and that KrasG12D serves a vital role in the control of tumor metabolism, through stimulation of glucose uptake and channeling of glucose intermediates through the hexosamine biosynthesis pathway (HBP) and the pentose phosphate pathway (PPP). Notably, these studies reveal that oncogenic Kras regulates ribose biogenesis. Unlike canonical models of PPP-mediated ribose biogenesis, we demonstrate that oncogenic Kras drives intermediates from enhanced glycolytic flux into the non-oxidative arm of the PPP, thereby decoupling ribose biogenesis from NADPNADPH-mediated redox control. Together, this work provides in vivo mechanistic insights into how oncogenic Kras promotes metabolic reprogramming in native tumors and illuminates potential metabolic targets that can be exploited for therapeutic benefit in Kras-driven PDAC.

Publication Title

Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE18064
Comparison of MBT/Pas and BALB/cByJ MEFs response after infection with Rift Valley Fever virus
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

The Rift Valley Fever (RVF) is an arthropod-borne disease present in several countries of Africa and Middle East. It is caused by RVF virus which can infect both humans and animals. In humans, it leads to various manifestations including hepatitis, encephalitis and death, while in domestic animals it usually causes miscarriage in pregnant females and it is often fatal for the newborn. Not all people or animal infected by the virus present the same disease. Some patients exhibit unapparent or moderate febrile reactions, while others develop severe symptoms. This observation suggests that host genetic factors play a role in controlling the outcome of infection. In this work, we compare the response of two different inbred strains of mice, MBT/Pas and BALB/cByJ, to infection with RVF virus. These strains exhibit different profiles of susceptibility to RVF virus infection. Indeed, MBT/Pas mice rapidly develop high viraemia and die soon after infection, while BALB/cByJ mice have a lower viraemia and die later. Interestingly, mouse embryonic fibroblasts (MEFs) obtained from MBT/Pas foetuses allows higher viral production than BALB/cByJ MEFs.

Publication Title

A new mouse model reveals a critical role for host innate immunity in resistance to Rift Valley fever.

Sample Metadata Fields

Specimen part

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accession-icon GSE56345
Therapeutic potential of spleen tyrosine kinase inhibition for treatment of high-risk precursor B-cell acute lymphoblastic leukemia
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

This study revealed pathogenic role of pre-BCR-independent SYK activation in high-risk B-ALL.

Publication Title

Therapeutic potential of spleen tyrosine kinase inhibition for treating high-risk precursor B cell acute lymphoblastic leukemia.

Sample Metadata Fields

Specimen part

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accession-icon GSE12134
The transcription factor AP2 regulates the number of basal progenitors
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon

Description

Understanding the mechanisms that specify neuronal subtypes is important to unravel the complex mechanisms of neuronal circuit assembly. Here we have identified a novel role for the transcription factor AP2 in progenitor and neuronal subtype specification in the cerebral cortex. Conditional deletion of AP2 causes misspecification of basal progenitors starting at

Publication Title

AP2gamma regulates basal progenitor fate in a region- and layer-specific manner in the developing cortex.

Sample Metadata Fields

No sample metadata fields

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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