Michael Leitges

WNT6/ACC2-induced storage of triacylglycerols in macrophages is exploited by Mycobacterium tuberculosis

Stromal cell protein kinase C-β inhibition enhances chemosensitivity in B cell malignancies and overcomes drug resistance

The kinase PKD3 provides negative feedback on cholesterol and triglyceride synthesis by suppressing insulin signaling

Protein Kinase C-β Dictates B Cell Fate by Regulating Mitochondrial Remodeling, Metabolic Reprogramming, and Heme Biosynthesis

High-Density Lipoproteins Exert Pro-inflammatory Effects on Macrophages via Passive Cholesterol Depletion and PKC-NF-κB/STAT1-IRF1 Signaling

Gain-of-function mutations in protein kinase Cα (PKCα) may promote synaptic defects in Alzheimer’s disease

Disruption of the PRKCD–FBXO25–HAX-1 axis attenuates the apoptotic response and drives lymphomagenesis

Renal PKC-ε deficiency attenuates acute kidney injury and ischemic allograft injury via TNF-α-dependent inhibition of apoptosis and inflammation

Protein Kinase Cδ Promotes Transitional B Cell-Negative Selection and Limits Proximal B Cell Receptor Signaling To Enforce Tolerance

PKCλ Haploinsufficiency Prevents Diabetes by a Mechanism Involving Alterations in Hepatic Enzymes

Wnt6 Is Expressed in Granulomatous Lesions of <i>Mycobacterium tuberculosis</i>–Infected Mice and Is Involved in Macrophage Differentiation and Proliferation

PKCβ Promotes Vascular Inflammation and Acceleration of Atherosclerosis in Diabetic ApoE Null Mice

aPKCλ/ι and aPKCζ Contribute to Podocyte Differentiation and Glomerular Maturation

Phenotypical Analysis of Atypical PKCs In Vivo Function Display a Compensatory System at Mouse Embryonic Day 7.5

Impairment of insulin-stimulated glucose transport and ERK activation by adipocyte-specific knockout of PKC-λ produces a phenotype characterized by diminished adiposity and enhanced insulin suppression of hepatic gluconeogenesis

Wnt6 Is Essential for Stromal Cell Proliferation During Decidualization in Mice1