R. Lindemann

发表

Ets1 is an effector of protein kinase Cα in cancer cells

C. Thomssen, S. Wesselborg, M. Vetter, 2005, Oncogene.

Interfering with TGFβ-induced Smad3 nuclear accumulation differentially affects TGFβ-dependent gene expression

A. Nordheim, J. Dittmer, R. Lindemann, 2003, Molecular Cancer.

Ets2 and protein kinase C epsilon are important regulators of parathyroid hormone-related protein expression in MCF-7 breast cancer cells.

C. Hauser, A. Nordheim, M. Braig, 2003, The Biochemical journal.

Image-based drug screen identifies HDAC inhibitors as novel Golgi disruptors synergizing with JQ1

J. Reiling, Jan Baumann, R. Lindemann, 2017, Molecular biology of the cell.

Golgi stress mediates redox imbalance and ferroptosis in human cells

S. Wölfl, J. Reiling, R. Lindemann, 2018, Communications Biology.

The BH3-Only Protein Bid Is Dispensable for DNA Damage- and Replicative Stress-Induced Apoptosis or Cell-Cycle Arrest

A. Strasser, P. Ekert, V. Dixit, 2007, Cell.

Ets1 is an effector of protein kinase Calpha in cancer cells.

C. Thomssen, S. Wesselborg, M. Vetter, 2005, Oncogene.

Protein kinase Calpha regulates Ets1 transcriptional activity in invasive breast cancer cells.

A. Nordheim, T. Guise, M. Braig, 2003, International journal of oncology.

The histone deacetylase inhibitors LAQ824 and LBH589 do not require death receptor signaling or a functional apoptosome to mediate tumor cell death or therapeutic efﬁcacy

Jessica E. Bolden, S. Lowe, A. Strasser, 2009 .

Cell survival and protein secretion associated with Golgi integrity in response to Golgi stress‐inducing agents

J. Reiling, H. Eggenweiler, R. Lindemann, 2017, Traffic.

Characterisation of the novel apoptotic and therapeutic activities of the histone deacetylase inhibitor romidepsin

R. Johnstone, L. Cluse, A. Dear, 2008, Molecular Cancer Therapeutics.

A Central Role for Bid in Granzyme B-induced Apoptosis*

J. Trapani, R. Johnstone, P. Bird, 2005, Journal of Biological Chemistry.

Combination therapy of established cancer using a histone deacetylase inhibitor and a TRAIL receptor agonist

Jessica E. Bolden, J. Bolden, R. Johnstone, 2008, Proceedings of the National Academy of Sciences.

Discovery and Structure–Activity Relationships of N‐Aryl 6‐Aminoquinoxalines as Potent PFKFB3 Kinase Inhibitors

M. Jurzak, M. Nowak, M. Kujawa, 2018, ChemMedChem.

Defining the target specificity of ABT-737 and synergistic antitumor activities in combination with histone deacetylase inhibitors.

R. Johnstone, A. Wiegmans, L. Cluse, 2009, Blood.

The mTORC1 inhibitor everolimus prevents and treats Eμ-Myc lymphoma by restoring oncogene-induced senescence.

S. Lowe, R. Pearson, G. McArthur, 2013, Cancer discovery.

cell death or therapeutic efficacy death receptor signaling or a functional apoptosome to mediate tumor The histone deacetylase inhibitors LAQ824 and LBH589 do not require

Jessica E. Bolden, S. Lowe, A. Strasser, 2010 .

The histone deacetylase inhibitors LAQ824 and LBH589 do not require death receptor signaling or a functional apoptosome to mediate tumor cell death or therapeutic efficacy.

Jessica E. Bolden, S. Lowe, A. Strasser, 2009, Blood.

TRAPPC13 modulates autophagy and the response to Golgi stress

J. Reiling, M. Starnbach, Jan Baumann, 2017, Journal of Cell Science.

Transforming Growth Factor β Regulates Parathyroid Hormone-related Protein Expression in MDA-MB-231 Breast Cancer Cells through a Novel Smad/Ets Synergism*

A. Nordheim, J. Dittmer, R. Lindemann, 2001, The Journal of Biological Chemistry.

Golgi stress–induced transcriptional changes mediated by MAPK signaling and three ETS transcription factors regulate MCL1 splicing

J. Reiling, Jan Baumann, R. Lindemann, 2018, Molecular biology of the cell.

Histone-Deacetylase Inhibitors for the Treatment of Cancer

R. Johnstone, B. Gabrielli, R. Lindemann, 2004, Cell cycle.

ATR represents a therapeutic vulnerability in clear cell renal cell carcinoma

P. Seidel, M. Boerries, D. von Elverfeldt, 2022, JCI insight.

Apoptotic Cells Induce Migration of Phagocytes via Caspase-3-Mediated Release of a Lipid Attraction Signal

S. Baksh, C. Belka, K. Schulze-Osthoff, 2003, Cell.

Secretory stressors induce intracellular death receptor accumulation to control apoptosis

J. Reiling, Bram J. van Raam, R. Lindemann, 2017, Cell Death and Disease.

Stroma-initiated hedgehog signaling takes center stage in B-cell lymphoma.

R. Lindemann, 2008, Cancer research.

Synthesis of amide and sulfonamide substituted N-aryl 6-aminoquinoxalines as PFKFB3 inhibitors with improved physicochemical properties.

M. Jurzak, M. Nowak, M. Kujawa, 2019, Bioorganic & medicinal chemistry letters.

HDAC inhibitors: magic bullets, dirty drugs or just another targeted therapy.

O. Witt, Olaf Witt, R. Lindemann, 2009, Cancer letters.

Analysis of the apoptotic and therapeutic activities of histone deacetylase inhibitors by using a mouse model of B cell lymphoma

Mark J. Smyth, Scott W. Lowe, Ricky W. Johnstone, 2007, Proceedings of the National Academy of Sciences.

Discovery and Structure-Activity Relationships of N-Aryl 6-Aminoquinoxalines as Potent PFKFB3 Kinase Inhibitors.

M. Jurzak, M. Nowak, M. Kujawa, 2018 .

Golgi stress mediates redox imbalance and ferroptosis in human cells

S. Wölfl, J. Reiling, R. Lindemann, 2018, Communications Biology.

Golgi stress mediates redox imbalance and ferroptosis in human cells

S. Wölfl, J. Reiling, R. Lindemann, 2018, Communications Biology.

Response: Does Bid Play a Role in the DNA Damage Response?

A. Strasser, P. Ekert, V. Dixit, 2007, Cell.

Discovery of Cycloalkyl[c]thiophenes as Novel Scaffolds for Hypoxia-Inducible Factor-2α Inhibitors.

M. Nowak, D. Musil, Liming Dong, 2023, Journal of medicinal chemistry.

The histone deacetylase inhibitors LAQ824 and LBH589 do not require death receptor signaling or a functional apoptosome to mediate tumor cell death or therapeutic efficacy.

Jessica E. Bolden, S. Lowe, A. Strasser, 2009, Blood.

Characterisation of the novel apoptotic and therapeutic activities of the histone deacetylase inhibitor romidepsin

R. Johnstone, L. Cluse, A. Dear, 2008, Molecular Cancer Therapeutics.