Pages that link to "Q48106714"
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The following pages link to Optic nerve glioma in mice requires astrocyte Nf1 gene inactivation and Nf1 brain heterozygosity. (Q48106714):
Displaying 50 items.
- Identification of a PTEN-regulated STAT3 brain tumor suppressor pathway (Q24650927) (← links)
- Tumor microenvironment and neurofibromatosis type I: connecting the GAPs (Q24654681) (← links)
- RASopathies: unraveling mechanisms with animal models (Q26800379) (← links)
- In vivo models of brain tumors: roles of genetically engineered mouse models in understanding tumor biology and use in preclinical studies (Q26820289) (← links)
- Eliminating barriers to personalized medicine: learning from neurofibromatosis type 1 (Q26828988) (← links)
- An integrative view on sex differences in brain tumors (Q26829861) (← links)
- A RASopathy gene commonly mutated in cancer: the neurofibromatosis type 1 tumour suppressor (Q27003534) (← links)
- MAPK pathway activation in pilocytic astrocytoma (Q27006028) (← links)
- Will kinase inhibitors make it as glioblastoma drugs? (Q27012684) (← links)
- The haploinsufficient hematopoietic microenvironment is critical to the pathological fracture repair in murine models of neurofibromatosis type 1 (Q27319893) (← links)
- Neurofibromin regulates neural stem cell proliferation, survival, and astroglial differentiation in vitro and in vivo (Q28504560) (← links)
- Oncogenic Kras expression in postmitotic neurons leads to S100A8-S100A9 protein overexpression and gliosis (Q28589373) (← links)
- Hyperactivation of p21ras and PI3K cooperate to alter murine and human neurofibromatosis type 1-haploinsufficient osteoclast functions (Q28593384) (← links)
- Optimizing biologically targeted clinical trials for neurofibromatosis. (Q30438898) (← links)
- Reduced striatal dopamine underlies the attention system dysfunction in neurofibromatosis-1 mutant mice. (Q30497049) (← links)
- Evidence of perturbations of cell cycle and DNA repair pathways as a consequence of human and murine NF1-haploinsufficiency (Q33544002) (← links)
- Defective cAMP generation underlies the sensitivity of CNS neurons to neurofibromatosis-1 heterozygosity (Q33831164) (← links)
- Targeting neovascular pericytes in neurofibromatosis type 1. (Q34016387) (← links)
- Mast cells and the neurofibroma microenvironment (Q34022409) (← links)
- Neurofibromin regulates corticostriatal inhibitory networks during working memory performance (Q34059456) (← links)
- Ultrastructural characterization of the optic pathway in a mouse model of neurofibromatosis-1 optic glioma (Q34079603) (← links)
- Neoplasms associated with germline and somatic NF1 gene mutations (Q34125947) (← links)
- Using the neurofibromatosis tumor predisposition syndromes to understand normal nervous system development (Q34176631) (← links)
- Sex Is a major determinant of neuronal dysfunction in neurofibromatosis type 1. (Q34231047) (← links)
- Neurofibromatosis type 1: modeling CNS dysfunction (Q34305314) (← links)
- Harnessing preclinical mouse models to inform human clinical cancer trials. (Q34498952) (← links)
- An 80-year experience with optic nerve glioma cases at the Armed Forces Institute of Pathology: evolution from museum to molecular evaluation suggests possibe interventions in the cellular senescence and microglial pathways (an American Ophthalmolog (Q34525316) (← links)
- Neurofibromatosis-1 heterozygosity increases microglia in a spatially and temporally restricted pattern relevant to mouse optic glioma formation and growth (Q34605219) (← links)
- Motivational disturbances and effects of L-dopa administration in neurofibromatosis-1 model mice. (Q34770412) (← links)
- The cyclic AMP pathway is a sex-specific modifier of glioma risk in type I neurofibromatosis patients. (Q34859935) (← links)
- Report from the fifth National Cancer Institute Mouse Models of Human Cancers Consortium Nervous System Tumors Workshop (Q35085344) (← links)
- Neurofibromatosis-1 regulates mTOR-mediated astrocyte growth and glioma formation in a TSC/Rheb-independent manner. (Q35229380) (← links)
- Somatic neurofibromatosis type 1 (NF1) inactivation events in cutaneous neurofibromas of a single NF1 patient (Q35310932) (← links)
- PET imaging for attention deficit preclinical drug testing in neurofibromatosis-1 mice. (Q35449276) (← links)
- Schweinfurthin A selectively inhibits proliferation and Rho signaling in glioma and neurofibromatosis type 1 tumor cells in a NF1-GRD-dependent manner. (Q35711858) (← links)
- The impact of coexisting genetic mutations on murine optic glioma biology. (Q35788566) (← links)
- Akt- or MEK-mediated mTOR inhibition suppresses Nf1 optic glioma growth (Q35788976) (← links)
- Review: insights gained from modelling high-grade glioma in the mouse (Q35854724) (← links)
- Skin-derived precursor cells as an in vitro modelling tool for the study of type 1 neurofibromatosis (Q35898391) (← links)
- Emerging insights into the molecular and cellular basis of glioblastoma (Q35914897) (← links)
- 3-D imaging mass spectrometry of protein distributions in mouse Neurofibromatosis 1 (NF1)-associated optic glioma. (Q35925481) (← links)
- Elucidating the impact of neurofibromatosis-1 germline mutations on neurofibromin function and dopamine-based learning (Q36008044) (← links)
- STAT3-iNOS Signaling Mediates EGFRvIII-Induced Glial Proliferation and Transformation (Q36130808) (← links)
- RNA Sequencing of Tumor-Associated Microglia Reveals Ccl5 as a Stromal Chemokine Critical for Neurofibromatosis-1 Glioma Growth. (Q36309612) (← links)
- Plexiform neurofibroma genesis: questions of Nf1 gene dose and hyperactive mast cells (Q36517090) (← links)
- Somatic neurofibromatosis type 1 (NF1) inactivation characterizes NF1-associated pilocytic astrocytoma (Q36660126) (← links)
- Reduced microglial CX3CR1 expression delays neurofibromatosis-1 glioma formation (Q36718351) (← links)
- Modeling cognitive dysfunction in neurofibromatosis-1 (Q36756183) (← links)
- Optic pathway gliomas in neurofibromatosis-1: controversies and recommendations. (Q36771546) (← links)
- Pediatric gliomas as neurodevelopmental disorders (Q36803476) (← links)