Gail V.W. Johnson

Does tissue transglutaminase play a role in Huntington's disease?

Mutant huntingtin aggregates do not sensitize cells to apoptotic stressors.

Direct, activating interaction between glycogen synthase kinase-3beta and p53 after DNA damage.

Cdk5 phosphorylates p53 and regulates its activity.

Tissue transglutaminase differentially modulates apoptosis in a stimuli-dependent manner.

Identification of the N-terminal functional domains of Cdk5 by molecular truncation and computer modeling.

Glycogen synthase kinase 3beta phosphorylates tau at both primed and unprimed sites. Differential impact on microtubule binding.

Axin negatively affects tau phosphorylation by glycogen synthase kinase 3beta.

Tau, where are we now?

Cystamine inhibits caspase activity. Implications for the treatment of polyglutamine disorders.

Transient osmotic stress facilitates mutant huntingtin aggregation.

Tissue transglutaminase directly regulates adenylyl cyclase resulting in enhanced cAMP-response element-binding protein (CREB) activation.

The p38 MAP kinase signaling pathway in Alzheimer's disease.

Mutant (R406W) human tau is hyperphosphorylated and does not efficiently bind microtubules in a neuronal cortical cell model.

Intracellular localization and activity state of tissue transglutaminase differentially impacts cell death.

Primed phosphorylation of tau at Thr231 by glycogen synthase kinase 3beta (GSK3beta) plays a critical role in regulating tau's ability to bind and stabilize microtubules.

Striatal cells from mutant huntingtin knock-in mice are selectively vulnerable to mitochondrial complex II inhibitor-induced cell death through a non-apoptotic pathway.

Immunoblot analysis reveals that isopeptide antibodies do not specifically recognize the epsilon-(gamma-glutamyl)lysine bonds formed by transglutaminase activity.

Cyclin-dependent kinase-5 in neurodegeneration.

Validity of mouse models for the study of tissue transglutaminase in neurodegenerative diseases.

Effects of cyclin-dependent kinase-5 activity on apoptosis and tau phosphorylation in immortalized mouse brain cortical cells.

The glamour and gloom of glycogen synthase kinase-3.

Mutant huntingtin directly increases susceptibility of mitochondria to the calcium-induced permeability transition and cytochrome c release.

Tissue transglutaminase is not involved in the aggregate formation of stably expressed alpha-synuclein in SH-SY5Y human neuroblastoma cells.

Glycogen synthase kinase 3 beta induces caspase-cleaved tau aggregation in situ.

FRAT-2 preferentially increases glycogen synthase kinase 3 beta-mediated phosphorylation of primed sites, which results in enhanced tau phosphorylation.

Tau phosphorylation in neuronal cell function and dysfunction.

Developmental regulation of tissue transglutaminase in the mouse forebrain.

Tissue transglutaminase contributes to disease progression in the R6/2 Huntington's disease mouse model via aggregate-independent mechanisms.

Tau phosphorylation: physiological and pathological consequences.

Transglutaminases in neurodegenerative disorders.

Role of the intracellular domains of LRP5 and LRP6 in activating the Wnt canonical pathway.

Verification of somatic CAG repeat expansion by pre-PCR fractionation.

The protective effects of cystamine in the R6/2 Huntington's disease mouse involve mechanisms other than the inhibition of tissue transglutaminase.

14-3-3Zeta does not increase GSK3beta-mediated tau phosphorylation in cell culture models.

Mitochondrial respiration and ATP production are significantly impaired in striatal cells expressing mutant huntingtin.

Increased glutathione levels in cortical and striatal mitochondria of the R6/2 Huntington's disease mouse model.

Cystamine treatment is neuroprotective in the YAC128 mouse model of Huntington disease.

The low density lipoprotein receptor-related protein 6 interacts with glycogen synthase kinase 3 and attenuates activity.

Tissue transglutaminase overexpression in the brain potentiates calcium-induced hippocampal damage.

Site-specific phosphorylation and caspase cleavage differentially impact tau-microtubule interactions and tau aggregation.

Tau phosphorylation and proteolysis: insights and perspectives.

Mutant huntingtin expression induces mitochondrial calcium handling defects in clonal striatal cells: functional consequences.

The role of tau phosphorylation and cleavage in neuronal cell death.

Transglutaminase 2 in neurodegenerative disorders.

Tau is hyperphosphorylated at multiple sites in mouse brain in vivo after streptozotocin-induced insulin deficiency.

The role of tau phosphorylation in the pathogenesis of Alzheimer's disease.

Regulated proteolytic processing of LRP6 results in release of its intracellular domain.

Mitochondrial-targeted active Akt protects SH-SY5Y neuroblastoma cells from staurosporine-induced apoptotic cell death.

Type 2 transglutaminase differentially modulates striatal cell death in the presence of wild type or mutant huntingtin.

Ubiquitin-proteasome system alterations in a striatal cell model of Huntington's disease.

Activation of glycogen synthase kinase 3beta promotes the intermolecular association of tau. The use of fluorescence resonance energy transfer microscopy.

Split GFP complementation assay: a novel approach to quantitatively measure aggregation of tau in situ: effects of GSK3beta activation and caspase 3 cleavage.

Transglutaminase 2 protects against ischemic insult, interacts with HIF1beta, and attenuates HIF1 signaling.

New application of beta-galactosidase complementation to monitor tau self-association.

Histone deacetylase 6 interacts with the microtubule-associated protein tau.

Rosiglitazone treatment prevents mitochondrial dysfunction in mutant huntingtin-expressing cells: possible role of peroxisome proliferator-activated receptor-gamma (PPARgamma) in the pathogenesis of Huntington disease.

The last tangle of tau.

Increased expression of Bim contributes to the potentiation of serum deprivation-induced apoptotic cell death in Huntington's disease knock-in striatal cell line.

Immortalized cortical neurons expressing caspase-cleaved tau are sensitized to endoplasmic reticulum stress induced cell death.

Caspase-cleaved tau expression induces mitochondrial dysfunction in immortalized cortical neurons: implications for the pathogenesis of Alzheimer disease.

Intracellular localization and conformational state of transglutaminase 2: implications for cell death.

Role of mitochondrial dysfunction in the pathogenesis of Huntington's disease.

Phosphorylation of PPP(S/T)P motif of the free LRP6 intracellular domain is not required to activate the Wnt/beta-catenin pathway and attenuate GSK3beta activity.

A caspase cleaved form of tau is preferentially degraded through the autophagy pathway.

The interrelationship between mitochondrial dysfunction and transcriptional dysregulation in Huntington disease.

Differential modulation of TCF/LEF-1 activity by the soluble LRP6-ICD.

The role of tau kinases in Alzheimer's disease.

AES/GRG5: more than just a dominant-negative TLE/GRG family member.

Split GFP complementation assay for quantitative measurement of tau aggregation in situ.

Cytosolic guanine nucledotide binding deficient form of transglutaminase 2 (R580a) potentiates cell death in oxygen glucose deprivation.

The toxicity of tau in Alzheimer disease: turnover, targets and potential therapeutics.

Truncated tau and Aβ cooperatively impair mitochondria in primary neurons.

Transglutaminase 2 and its role in pulmonary fibrosis.

Decreases in valosin-containing protein result in increased levels of tau phosphorylated at Ser262/356.

Transglutaminase 2: A molecular Swiss army knife.

Complete transglutaminase 2 ablation results in reduced stroke volumes and astrocytes that exhibit increased survival in response to ischemia.

Metabolic State Determines Sensitivity to Cellular Stress in Huntington Disease: Normalization by Activation of PPARγ.