Ellen Cahir-McFarland
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View article: Maintenance of chronic neuroinflammation in multiple sclerosis via interferon signaling and CD8 T-cell-mediated cytotoxicity
Maintenance of chronic neuroinflammation in multiple sclerosis via interferon signaling and CD8 T-cell-mediated cytotoxicity Open
Chronic neuroinflammation and neurodegeneration are critical but unresolved drivers of disability accumulation in progressive multiple sclerosis (MS). Chronic active white matter lesions, identifiable radiologically as paramagnetic rim les…
View article: Maintenance of chronic neuroinflammation in multiple sclerosis via interferon signaling and CD8 T cell-mediated cytotoxicity
Maintenance of chronic neuroinflammation in multiple sclerosis via interferon signaling and CD8 T cell-mediated cytotoxicity Open
Chronic neuroinflammation and neurodegeneration are critical but unresolved drivers of disability accumulation in progressive multiple sclerosis (MS). Chronic active white matter lesions (CAL), identifiable radiologically as paramagnetic r…
View article: Supplementary Figure 2 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Supplementary Figure 2 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
PDF file - 478K
View article: Supplementary Figure 4 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Supplementary Figure 4 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
PDF file - 314K
View article: Supplementary Figure 1A-G from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Supplementary Figure 1A-G from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
PDF file - 524K
View article: Supplementary Figure 3 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Supplementary Figure 3 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
PDF file - 381K
View article: Supplementary Figure 2 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Supplementary Figure 2 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
PDF file - 478K
View article: Data from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Data from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
All cancer cells require increased nutrient uptake to support proliferation. In this study, we investigated the signals that govern glucose uptake in B-cell lymphomas and determined that the inhibitor of NF-κB-kinase β (IKKβ) induced gluco…
View article: Data from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Data from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
All cancer cells require increased nutrient uptake to support proliferation. In this study, we investigated the signals that govern glucose uptake in B-cell lymphomas and determined that the inhibitor of NF-κB-kinase β (IKKβ) induced gluco…
View article: Supplementary Figure 1A-G from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Supplementary Figure 1A-G from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
PDF file - 524K
View article: Supplementary Figure Legends 1-4, Methods from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Supplementary Figure Legends 1-4, Methods from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
PDF file - 84K
View article: Supplementary Figure 4 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Supplementary Figure 4 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
PDF file - 314K
View article: Supplementary Figure 1H-N from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Supplementary Figure 1H-N from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
PDF file - 569K
View article: Supplementary Figure 3 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Supplementary Figure 3 from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
PDF file - 381K
View article: Supplementary Figure Legends 1-4, Methods from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Supplementary Figure Legends 1-4, Methods from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
PDF file - 84K
View article: Supplementary Figure 1H-N from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1
Supplementary Figure 1H-N from IKKβ and NF-κB Transcription Govern Lymphoma Cell Survival through AKT-Induced Plasma Membrane Trafficking of GLUT1 Open
PDF file - 569K
View article: Pharmacokinetic and Target Engagement Measures of ANX007, an Anti-C1q Antibody Fragment, Following Intravitreal Administration in Nonhuman Primates
Pharmacokinetic and Target Engagement Measures of ANX007, an Anti-C1q Antibody Fragment, Following Intravitreal Administration in Nonhuman Primates Open
Following IVT administration, ANX007 distributes to sites within the retina that are relevant to neurodegenerative ophthalmic disease with clear evidence of C1q target engagement. Based on its mechanism of action inhibiting C1q and its dow…
View article: OP0232 HIGH PLASMA C4d/C4 IDENTIFIES LUPUS NEPHRITIS PATIENTS WITH DISEASE MEDIATED BY ACTIVATION OF THE CLASSICAL COMPLEMENT PATHWAY
OP0232 HIGH PLASMA C4d/C4 IDENTIFIES LUPUS NEPHRITIS PATIENTS WITH DISEASE MEDIATED BY ACTIVATION OF THE CLASSICAL COMPLEMENT PATHWAY Open
View article: Pharmacokinetics and target engagement of intravitreal administration of ANX007, an anti-C1q antibody fragment, in nonhuman primates
Pharmacokinetics and target engagement of intravitreal administration of ANX007, an anti-C1q antibody fragment, in nonhuman primates Open
View article: MOG autoantibodies trigger a tightly-controlled FcR and BTK-driven microglia proliferative response
MOG autoantibodies trigger a tightly-controlled FcR and BTK-driven microglia proliferative response Open
Autoantibodies are a hallmark of numerous neurological disorders, including multiple sclerosis, autoimmune encephalitides and neuromyelitis optica. Whilst well understood in peripheral myeloid cells, the pathophysiological significance of …
View article: Abnormalities in normal-appearing white matter from which multiple sclerosis lesions arise
Abnormalities in normal-appearing white matter from which multiple sclerosis lesions arise Open
Normal-appearing white matter is far from normal in multiple sclerosis; little is known about the precise pathology or spatial pattern of this alteration and its relation to subsequent lesion formation. This study was undertaken to evaluat…
View article: Patterning Chronic Active Demyelination in Slowly Expanding/Evolving White Matter MS Lesions
Patterning Chronic Active Demyelination in Slowly Expanding/Evolving White Matter MS Lesions Open
Patterns of longitudinal change in the normalized magnetization transfer ratio and DTI radial diffusivity in slowly expanding/evolving lesions were consistent with progressive demyelination and tissue loss, as seen in smoldering white matt…
View article: Cell-autonomous and non-cell autonomous effects of neuronal BIN1 loss in vivo
Cell-autonomous and non-cell autonomous effects of neuronal BIN1 loss in vivo Open
BIN1 is the most important risk locus for Late Onset Alzheimer's Disease (LOAD), after ApoE. BIN1 AD-associated SNPs correlate with Tau deposition as well as with brain atrophy. Furthermore, the level of neuronal-specific BIN1 isoform 1 pr…
View article: BIN1 favors the spreading of Tau via extracellular vesicles
BIN1 favors the spreading of Tau via extracellular vesicles Open
Despite Bridging INtegrator 1 ( BIN1 ) being the second most statistically-significant locus associated to Late Onset Alzheimer’s Disease, its role in disease pathogenesis remains to be clarified. As reports suggest a link between BIN1, Ta…
View article: Epstein-Barr-Virus-Induced One-Carbon Metabolism Drives B Cell Transformation
Epstein-Barr-Virus-Induced One-Carbon Metabolism Drives B Cell Transformation Open
Epstein-Barr virus (EBV) causes Burkitt, Hodgkin, and post-transplant B cell lymphomas. How EBV remodels metabolic pathways to support rapid B cell outgrowth remains largely unknown. To gain insights, primary human B cells were profiled by…
View article: Identification of regulators of the myofibroblast phenotype of primary dermal fibroblasts from early diffuse systemic sclerosis patients
Identification of regulators of the myofibroblast phenotype of primary dermal fibroblasts from early diffuse systemic sclerosis patients Open
View article: Polyomavirus T Antigen Induces <i>APOBEC3B</i> Expression Using an LXCXE-Dependent and TP53-Independent Mechanism
Polyomavirus T Antigen Induces <i>APOBEC3B</i> Expression Using an LXCXE-Dependent and TP53-Independent Mechanism Open
The APOBEC3B DNA cytosine deaminase is overexpressed in many different cancers and correlates with elevated frequencies of C-to-T and C-to-G mutations in 5′-TC motifs, oncogene activation, acquired drug resistance, and poor clinical outcom…
View article: A Novel Panel of Rabbit Monoclonal Antibodies and Their Diverse Applications Including Inhibition of Clostridium perfringens Epsilon Toxin Oligomerization
A Novel Panel of Rabbit Monoclonal Antibodies and Their Diverse Applications Including Inhibition of Clostridium perfringens Epsilon Toxin Oligomerization Open
The pore-forming epsilon toxin (ETX) produced by Clostridium perfringens is among the most lethal bacterial toxins known. Sensitive antibody-based reagents are needed to detect toxin, distinguish mechanisms of cell death, and prevent ETX t…
View article: Polyomavirus T-Antigen Induces<i>APOBEC3B</i>Expression using a LXCXE-Dependent and TP53-Independent Mechanism
Polyomavirus T-Antigen Induces<i>APOBEC3B</i>Expression using a LXCXE-Dependent and TP53-Independent Mechanism Open
APOBEC3B is a single-stranded DNA cytosine deaminase with beneficial innate antiviral functions. However, misregulated APOBEC3B can also be detrimental by inflicting APOBEC signature C-to-T and C-to-G mutations in genomic DNA of multiple c…
View article: Investigating small molecules to inhibit germinal center kinase-like kinase (GLK/MAP4K3) upstream of PKCθ phosphorylation: Potential therapy to modulate T cell dependent immunity
Investigating small molecules to inhibit germinal center kinase-like kinase (GLK/MAP4K3) upstream of PKCθ phosphorylation: Potential therapy to modulate T cell dependent immunity Open