M. Lienhard Schmitz

Controlling NF-kappaB activation in T cells by costimulatory receptors.

Autoregulatory control of the p53 response by caspase-mediated processing of HIPK2.

Roles of HIPK1 and HIPK2 in AML1- and p300-dependent transcription, hematopoiesis and blood vessel formation.

Phosphorylation-dependent control of Pc2 SUMO E3 ligase activity by its substrate protein HIPK2.

HIPK2: a versatile switchboard regulating the transcription machinery and cell death.

NF-kappaB inhibitors for the treatment of inflammatory diseases and cancer.

NIK and Cot cooperate to trigger NF-kappaB p65 phosphorylation.

A bacterial small molecule undermining immune response signaling.

Functional architecture of the cell nucleus.

An inducible autoregulatory loop between HIPK2 and Siah2 at the apex of the hypoxic response.

Autoregulatory feedback loops terminating the NF-kappaB response.

Activation of T cells: releasing the brakes by proteolytic elimination of Cbl-b.

SUMOylation-dependent localization of IKKepsilon in PML nuclear bodies is essential for protection against DNA-damage-triggered cell death.

Specification of the NF-kappaB transcriptional response by p65 phosphorylation and TNF-induced nuclear translocation of IKK epsilon.

Control of nuclear HIPK2 localization and function by a SUMO interaction motif.

Regulation of NF-κB activity by competition between RelA acetylation and ubiquitination.

Signal integration, crosstalk mechanisms and networks in the function of inflammatory cytokines.

A redox-regulated SUMO/acetylation switch of HIPK2 controls the survival threshold to oxidative stress.

HIPK2 kinase activity depends on cis-autophosphorylation of its activation loop.

SIAH-mediated ubiquitination and degradation of acetyl-transferases regulate the p53 response and protein acetylation.

The coactivator role of histone deacetylase 3 in IL-1-signaling involves deacetylation of p65 NF-κB.

Regulation of the tumor suppressor PML by sequential post-translational modifications.

Cyclin-dependent kinase 6 phosphorylates NF-κB P65 at serine 536 and contributes to the regulation of inflammatory gene expression.

Posttranslational modifications regulate HIPK2, a driver of proliferative diseases.

Homeodomain-interacting protein kinase 2-dependent repression of myogenic differentiation is relieved by its caspase-mediated cleavage.

Hsc70 is a novel interactor of NF-kappaB p65 in living hippocampal neurons.

The cytokine-induced conformational switch of nuclear factor κB p65 is mediated by p65 phosphorylation.

Cyclin-dependent kinase 6 is a chromatin-bound cofactor for NF-κB-dependent gene expression.

Expression pattern of protease activated receptors in lymphoid cells.

The intricate interplay between RNA viruses and NF-κB.

SUMO modification of TBK1 at the adaptor-binding C-terminal coiled-coil domain contributes to its antiviral activity.

The Activation of IL-1-Induced Enhancers Depends on TAK1 Kinase Activity and NF-κB p65.

Cyclin-Dependent Kinases as Coregulators of Inflammatory Gene Expression.

HIPK family kinases bind and regulate the function of the CCR4-NOT complex.

SUMO5, a Novel Poly-SUMO Isoform, Regulates PML Nuclear Bodies.

K63-Ubiquitylation and TRAF6 Pathways Regulate Mammalian P-Body Formation and mRNA Decapping.

The Influenza A Virus Genotype Determines the Antiviral Function of NF-κB.

Testing the Effects of SIAH Ubiquitin E3 Ligases on Lysine Acetyl Transferases.

The NF-κB-dependent and -independent transcriptome and chromatin landscapes of human coronavirus 229E-infected cells.

The CCR4-NOT complex contributes to repression of Major Histocompatibility Complex class II transcription.

NF-κB p65 serine 467 phosphorylation sensitizes mice to weight gain and TNFα-or diet-induced inflammation.

The Direct and Indirect Roles of NF-κB in Cancer: Lessons from Oncogenic Fusion Proteins and Knock-in Mice.