D. Grubb

发表

Tissue-specific splicing of an Ndufs6 gene-trap insertion generates a mitochondrial complex I deficiency-specific cardiomyopathy

Michael T Ryan, Joseph J Smolich, Michael Lazarou, 2012, Proceedings of the National Academy of Sciences.

Conformational control of Bax localization and apoptotic activity by Pro168

C. Borner, A. Schinzel, M. Schuler, 2004, The Journal of cell biology.

Unspecific activation of caspases during the induction of apoptosis by didemnin B in human cell lines

A. Lawen, D. Grubb, K. L. Johnson, 1999, Journal of cellular biochemistry.

Scaffolding protein Homer 1c mediates hypertrophic responses downstream of Gq in cardiomyocytes

E. Woodcock, D. Grubb, J. Luo, 2012, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

Selective activation of the "b" splice variant of phospholipase Cbeta1 in chronically dilated human and mouse atria.

A. Dart, T. Filtz, J. Sadoshima, 2009, Journal of molecular and cellular cardiology.

Gq‐initiated cardiomyocyte hypertrophy is mediated by phospholipase Cβ1b

T. Filtz, E. Woodcock, D. Grubb, 2009, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

Resistance of melanoma cell lines to interferons correlates with reduction of IFN-induced tyrosine phosphorylation. Induction of the anti-viral state by IFN is prevented by tyrosine kinase inhibitors.

B. Wines, S. Ralph, A. Linnane, 1995, Journal of immunology.

Expressing an inhibitor of PLCβ1b sustains contractile function following pressure overload.

E. Woodcock, Xiao-Ming Gao, Xiaojun Du, 2016, Journal of Molecular and Cellular Cardiology.

Didemnin B induces apoptosis in proliferating but not resting peripheral blood mononuclear cells

M. Baker, A. Lawen, D. Grubb, 2002, Apoptosis.

The extreme C‐terminal region of phospholipase Cβ1 determines subcellular localization and function; the “b” splice variant mediates α1‐adrenergic receptor responses in cardiomyocytes

H. Huynh, E. Woodcock, D. Grubb, 2008, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

The atypical 'b' splice variant of phospholipase Cβ1 promotes cardiac contractile dysfunction.

E. Woodcock, Xiao-Ming Gao, Xiaojun Du, 2015, Journal of molecular and cellular cardiology.

Phospholipase Cβlb associates with a Shank3 complex at the cardiac sarcolemma

P. Iliades, T. Filtz, E. Woodcock, 2011, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

Phospholipase Cβ1b directly binds the SH3 domain of Shank3 for targeting and activation in cardiomyocytes.

E. Woodcock, D. Grubb, Jieting Luo, 2015, Biochemical and biophysical research communications.

Didemnin B induces cell death by apoptosis: the fastest induction of apoptosis ever described.

E. Wolvetang, A. Lawen, D. Grubb, 1995, Biochemical and biophysical research communications.

The mitochondrial membrane potential (Δψm) in apoptosis; an update

J. Ly, A. Lawen, D. Grubb, 2003, Apoptosis.

Mitochondrial cytochrome c release is caspase-dependent and does not involve mitochondrial permeability transition in didemnin B-induced apoptosis

J. Ly, F. Vaillant, A. Lawen, 2001, Oncogene.

Regulation of autophagy in cardiomyocytes by Ins(1,4,5)P(3) and IP(3)-receptors.

E. Woodcock, D. Grubb, Jieting Luo, 2013, Journal of molecular and cellular cardiology.

The mitochondrial membrane potential (deltapsi(m)) in apoptosis; an update.

J. Ly, A. Lawen, D. Grubb, 2003, Apoptosis : an international journal on programmed cell death.

Ins(1,4,5)P(3) regulates phospholipase Cbeta1 expression in cardiomyocytes.

T. Filtz, E. Woodcock, Ju Chen, 2008, Journal of molecular and cellular cardiology.

Novel Therapeutic Targets in Heart Failure: The Phospholipase Cβ1b–Shank3 Interface

E. Woodcock, D. Grubb, 2015 .

Chronic Contractile Dysfunction without Hypertrophy Does Not Provoke a Compensatory Transcriptional Response in Mouse Hearts

E. Woodcock, J. McMullen, S. Matkovich, 2016, PloS one.

Potential treatment of cardiac hypertrophy and heart failure by inhibiting the sarcolemmal binding of phospholipase Cbeta1b.

P. Iliades, E. Woodcock, D. Grubb, 2010, Current drug targets.

The Phosphatidylinositol(4,5)Bisphosphate–Binding Sequence of Transient Receptor Potential Channel Canonical 4α Is Critical for Its Contribution to Cardiomyocyte Hypertrophy

E. Woodcock, D. Grubb, Jieting Luo, 2014, Molecular Pharmacology.