Michael Susithiran Samuel

Scopus Publications

Compressive stress–driven Piezo1 activation and Rho-ROCK mechanotransduction promote tumor progression via epigenetic mechanical memory
Sarah T. Boyle, David Gallego-Ortega, Edward J. Buckley, Emmanuelle Cognard, M. Zahied Johan, et al.
Science Advances, 2026
Rapidly growing tumors experience high tissue-level forces, particularly when growing within a restricted space. These require counteracting by intracellular forces to prevent tissue damage. Here, we reveal the ion channel Piezo1 as a mechanosensor of compressive force, activating Rho–Rho kinase (ROCK) mechanotransduction to generate intracellular forces and enhancing malignant characteristics of tumors. Compressive stress promoted cancer growth in vivo in a Rho-ROCK–dependent manner. Silencing Piezo1 abolished compression-induced Rho-ROCK activation and tumor progression in this model. Accordingly, elevated PIEZO1 is associated with 35% poorer survival of patients with breast cancer. We show that acute compressive forces engender epigenetic mechanical memory via Piezo1-activated Rho-ROCK signaling, promoting tumor growth in vivo. Compressive stress promoted ROCK-dependent histone modifications associated with open chromatin, including acetylation of key histone 3–lysine residues, regulating the expression of cancer-related genes across cell, explant, and in vivo tumor models. Our observations suggest that the PIEZO1-RHO-ROCK axis links tissue-level forces to persistent tumor-promoting epigenetic changes and merits evaluation as a mechanotherapy target in cancer.
Enhanced RHO-ROCK signaling is associated with CRELD2 production and fibroblast recruitment in cutaneous squamous cell carcinoma
Alexandra Pittar, Edward J. Buckley, Sarah T. Boyle, S. Jan Ibbetson, Michael S. Samuel
Cytoskeleton, 2024
A key characteristic of cancer cells is their ability to induce changes in their microenvironment that render it permissive to tumor growth, invasion and metastasis. Indeed, these changes are required for tumor progression. Consequently, the tumor microenvironment is emerging as a key source of new targets against cancer, with novel therapies aimed at reversing tumor‐promoting changes, reinstating a tumor‐hostile microenvironment and suppressing disease progression. RHO‐ROCK signaling, and consequent tension within the cellular actomyosin cytoskeleton, regulates a paracrine signaling cascade that establishes a tumor‐promoting microenvironment. Here, we show that consistent with our observations in breast cancer, enhanced ROCK activity and consequent production of CRELD2 is associated with the recruitment and tumor‐promoting polarization of cancer‐associated fibroblasts in cutaneous squamous cell carcinoma. Our observations provide support for the notion that the role of RHO‐ROCK signaling in establishing a tumor‐promoting microenvironment may be conserved across patients and potentially also different cancer types.
Accelerated Closure of Diabetic Wounds by Efficient Recruitment of Fibroblasts upon Inhibiting a 14-3-3/ROCK Regulatory Axis
M. Zahied Johan, Natasha T. Pyne, Natasha Kolesnikoff, Valentina Poltavets, Zahra Esmaeili, et al.
Journal of Investigative Dermatology, 2024
Temporally resolved proteomics identifies nidogen-2 as a cotarget in pancreatic cancer that modulates fibrosis and therapy response
Brooke A. Pereira, Shona Ritchie, Cecilia R. Chambers, Katie A. Gordon, Astrid Magenau, et al.
Science Advances, 2024
Pancreatic ductal adenocarcinoma (PDAC) is characterized by increasing fibrosis, which can enhance tumor progression and spread. Here, we undertook an unbiased temporal assessment of the matrisome of the highly metastatic KPC ( Pdx1-Cre , LSL-Kras G12D/+ , LSL-Trp53 R172H/+ ) and poorly metastatic KP fl C ( Pdx1-Cre , LSL-Kras G12D/+ , Trp53 fl/+ ) genetically engineered mouse models of pancreatic cancer using mass spectrometry proteomics. Our assessment at early-, mid-, and late-stage disease reveals an increased abundance of nidogen-2 (NID2) in the KPC model compared to KP fl C, with further validation showing that NID2 is primarily expressed by cancer-associated fibroblasts (CAFs). Using biomechanical assessments, second harmonic generation imaging, and birefringence analysis, we show that NID2 reduction by CRISPR interference (CRISPRi) in CAFs reduces stiffness and matrix remodeling in three-dimensional models, leading to impaired cancer cell invasion. Intravital imaging revealed improved vascular patency in live NID2-depleted tumors, with enhanced response to gemcitabine/Abraxane. In orthotopic models, NID2 CRISPRi tumors had less liver metastasis and increased survival, highlighting NID2 as a potential PDAC cotarget.
Erratum: Actomyosin-Mediated Cellular Tension Drives Increased Tissue Stiffness and β-Catenin Activation to Induce Epidermal Hyperplasia and Tumor Growth (Cancer Cell (2011) 19(6) (776–791), (S1535610811001668), (10.1016/j.ccr.2011.05.008))
Michael S. Samuel, Jose I. Lopez, Ewan J. McGhee, Daniel R. Croft, David Strachan, et al.
Cancer Cell, 2024
An orthotopic syngeneic mouse model of bortezomib-resistant multiple myeloma
Manjun Li, Melissa K. Bennett, John Toubia, Victoria S. Pope, Melinda N. Tea, et al.
British Journal of Haematology, 2024
SummaryWhile bortezomib has significant benefits in multiple myeloma (MM) therapy, the disease remains incurable due to the invariable development of bortezomib resistance. This emphasises the need for advanced models for preclinical evaluation of new therapeutic approaches for bortezomib‐resistant MM. Here, we describe the development of an orthotopic syngeneic bortezomib‐resistant MM mouse model based on the most well‐characterised syngeneic MM mouse model derived from spontaneous MM‐forming C57BL/KaLwRij mice. Using bortezomib‐resistant 5TGM1 cells, we report and characterise a robust syngeneic mouse model of bortezomib‐resistant MM that is well suited to the evaluation of new therapeutic approaches for proteasome inhibitor‐resistant MM.
Basonuclin-2 regulates extracellular matrix production and degradation
Ayla Orang, B Kate Dredge, Chi Yau Liu, Julie M Bracken, Chun-Hsien Chen, et al.
Life Science Alliance, 2023
Epithelial–mesenchymal transition is essential for tissue patterning and organization. It involves both regulation of cell motility and alterations in the composition and organization of the ECM—a complex environment of proteoglycans and fibrous proteins essential for tissue homeostasis, signaling in response to chemical and biomechanical stimuli, and is often dysregulated under conditions such as cancer, fibrosis, and chronic wounds. Here, we demonstrate that basonuclin-2 (BNC2), a mesenchymal-expressed gene, that is, strongly associated with cancer and developmental defects across genome-wide association studies, is a novel regulator of ECM composition and degradation. We find that at endogenous levels, BNC2 controls the expression of specific collagens, matrix metalloproteases, and other matrisomal components in breast cancer cells, and in fibroblasts that are primarily responsible for the production and processing of the ECM within the tumour microenvironment. In so doing, BNC2 modulates the motile and invasive properties of cancers, which likely explains the association of high BNC2 expression with increasing cancer grade and poor patient prognosis.
Bevacizumab-Induced Hypertension in Glioblastoma Patients and Its Potential as a Modulator of Treatment Response
Kaitlin G. Scheer, Lisa M. Ebert, Michael S. Samuel, Claudine S. Bonder, Guillermo A. Gomez
Hypertension, 2023
Glioblastoma invasion is the primary mechanism responsible for its dismal prognosis and is the direct result of interactions between glioblastoma cells and the tumor vasculature. The dysregulated microvasculature in glioblastoma tumors and vessels co-opted from surrounding brain tissue support rapid tumor growth and are utilized as pathways for invasive cancer cells. Attempts to target the glioblastoma vasculature with antiangiogenic agents (eg, bevacizumab) have nonetheless shown limited and inconsistent efficacy, and the underlying causes of such heterogeneous responses remain unknown. Several studies have identified that patients with glioblastoma who develop hypertension following treatment with bevacizumab show significant improvement in overall survival compared with normotensive nonresponders. Here we review these findings and discuss the potential of hypertension as a biomarker for glioblastoma treatment response in individual patients and the role of hypertension as a modulator of interactions between tumor cells and cells in the perivascular niche. We suggest that a better understanding of the actions of bevacizumab and hypertension at the cellular level will contribute to developing more effective personalized therapies that address glioblastoma tumor cell invasion.
An interview with Michael Samuel - Tumour Microenvironment Laboratory, Centre for Cancer Biology, SA Pathology and University of South Australia
Michael S. Samuel, Lena Van, Paul Trevorrow
Cytoskeleton, 2023
We work on the tumour microenvironment: that is, everything in a tumour mass that is not the tumour cells themselves. My group is interested in how tumour cells hijack their environment to cause progression of the disease. There has been a lot of effort over many years, particularly in targeting immune cells within the microenvironment, but there are other aspects of the microenvironment that could also be targeted. We are working on how changes in the cytoskeleton in tumour cells influences the remodelling of the microenvironment, such that it becomes permissive for cancer growth. For instance, how changes in the cytoskeleton in tumour cells makes the extracellular matrix of the microenvironment stiffer and therefore easier for tumour-promoting cancer-associated fibroblasts to invade in or more difficult for tumour-suppressive immune cells to invade in. We think that some of these changes in the cytoskeleton permit the more deleterious aspects of the tumour microenvironment to flourish. The idea is, of course, that we can stop this from happening by targeting the cytoskeleton and the consequences of such cytoskeletal changes, to help patients.
Actomyosin-mediated cellular tension promotes Yap nuclear translocation and myocardial proliferation through α5 integrin signaling
Xiaofei Li, Callie McLain, Michael S. Samuel, Michael F. Olson, Glenn L. Radice
Development Cambridge, 2023
The cardiomyocyte phenotypic switch from a proliferative to terminally differentiated state results in the loss of regenerative potential of the mammalian heart shortly after birth. Nonmuscle myosin IIB (NM IIB)-mediated actomyosin contractility regulates cardiomyocyte cytokinesis in the embryonic heart, and NM IIB levels decline after birth, suggesting a role for cellular tension in the regulation of cardiomyocyte cell cycle activity in the postnatal heart. To investigate the role of actomyosin contractility in cardiomyocyte cell cycle arrest, we conditionally activated ROCK2 kinase domain (ROCK2:ER) in the murine postnatal heart. Here, we show that α5/β1 integrin and fibronectin matrix increase in response to actomyosin-mediated tension. Moreover, activation of ROCK2:ER promotes nuclear translocation of Yap, a mechanosensitive transcriptional co-activator, and enhances cardiomyocyte proliferation. Finally, we show that reduction of myocardial α5 integrin rescues the myocardial proliferation phenotype in ROCK2:ER hearts. These data demonstrate that cardiomyocytes respond to increased intracellular tension by altering their intercellular contacts in favor of cell–matrix interactions, leading to Yap nuclear translocation, thus uncovering a function for nonmuscle myosin contractility in promoting cardiomyocyte proliferation in the postnatal heart.
Desmoglein-2 as a cancer modulator: friend or foe?
Kay K. Myo Min, Charlie B. Ffrench, Barbara J. McClure, Michael Ortiz, Emma L. Dorward, et al.
Frontiers in Oncology, 2023
ALTEN: A High-Fidelity Primary Tissue-Engineering Platform to Assess Cellular Responses Ex Vivo
Andrew M. K. Law, Jiamin Chen, Yolanda Colino‐Sanguino, Laura Rodriguez de la Fuente, Guocheng Fang, et al.
Advanced Science, 2022
Nano-Mechanical Analyses of Native and Cross-Linked Collagen I Matrices Reveal the Mechanical Complexity of Homogenous Samples
Brock Alan Le Cerf, Natasha Theresa Pyne, Jasreen Kular, Sarah Theresa Boyle, David Allan Beattie, et al.
Frontiers in Physics, 2022
Differentiation of the tumor microenvironment: are CAFs the Organizer?
Marina Kochetkova, Michael Susithiran Samuel
Trends in Cell Biology, 2022
Interrelationships between the extracellular matrix and the immune microenvironment that govern epithelial tumour progression
Natasha Kolesnikoff, Chun-Hsien Chen, Michael Susithiran Samuel
Clinical Science, 2022
Tumour-directed microenvironment remodelling at a glance
Sarah T. Boyle, M. Zahied Johan, Michael S. Samuel
Journal of Cell Science, 2021
Intravital imaging technology guides FAK-mediated priming in pancreatic cancer precision medicine according to Merlin status
Kendelle J. Murphy, Daniel A. Reed, Claire Vennin, James R. W. Conway, Max Nobis, et al.
Science Advances, 2021
Optimizing metastatic-cascade-dependent Rac1 targeting in breast cancer: Guidance using optical window intravital FRET imaging
Alessia Floerchinger, Kendelle J. Murphy, Sharissa L. Latham, Sean C. Warren, Andrew T. McCulloch, et al.
Cell Reports, 2021
A deep convolutional neural network for segmentation of whole-slide pathology images identifies novel tumour cell-perivascular niche interactions that are associated with poor survival in glioblastoma
Amin Zadeh Shirazi, Mark D. McDonnell, Eric Fornaciari, Narjes Sadat Bagherian, Kaitlin G. Scheer, et al.
British Journal of Cancer, 2021
Mechanical Signaling in the Mammary Microenvironment: From Homeostasis to Cancer
Sarah Theresa Boyle, Valentina Poltavets, Michael Susithiran Samuel
Advances in Experimental Medicine and Biology, 2021
Systemic Delivery of Anti-Integrin αl Antibodies Reduces Early Macrophage Recruitment, Inflammation, and Scar Formation in Murine Burn Wounds
Xanthe L. Strudwick, Damian H. Adams, Natasha T. Pyne, Michael S. Samuel, Rachael Z. Murray, et al.
Advances in Wound Care, 2020
Uncovering tumor-stroma inter-relationships using MALDI mass spectrometry imaging
Sarah T. Boyle, Parul Mittal, Gurjeet Kaur, Peter Hoffmann, Michael S. Samuel, et al.
Journal of Proteome Research, 2020
Acute compressive stress activates RHO/ROCK-mediated cellular processes
Sarah T. Boyle, Jasreen Kular, Max Nobis, Andrew Ruszkiewicz, Paul Timpson, et al.
Small Gtpases, 2020
ROCK-mediated selective activation of PERK signalling causes fibroblast reprogramming and tumour progression through a CRELD2-dependent mechanism
Sarah Theresa Boyle, Valentina Poltavets, Jasreen Kular, Natasha Theresa Pyne, Jarrod John Sandow, et al.
Nature Cell Biology, 2020
Publisher Correction: ROCK-mediated selective activation of PERK signalling causes fibroblast reprogramming and tumour progression through a CRELD2-dependent mechanism (Nature Cell Biology, (2020), 22, 7, (882-895), 10.1038/s41556-020-0523-y)
Sarah Theresa Boyle, Valentina Poltavets, Jasreen Kular, Natasha Theresa Pyne, Jarrod John Sandow, et al.
Nature Cell Biology, 2020
Cytoplasmic dynein regulates the subcellular localization of sphingosine kinase 2 to elicit tumor-suppressive functions in glioblastoma
Heidi A. Neubauer, Melinda N. Tea, Julia R. Zebol, Briony L. Gliddon, Cassandra Stefanidis, et al.
Oncogene, 2019
Glioblastoma heterogeneity and the tumour microenvironment: Implications for preclinical research and development of new treatments
Sally L. Perrin, Michael S. Samuel, Barbara Koszyca, Michael P. Brown, Lisa M. Ebert, et al.
Biochemical Society Transactions, 2019
Targeting stromal remodeling and cancer stem cell plasticity overcomes chemoresistance in triple negative breast cancer
Aurélie S. Cazet, Mun N. Hui, Benjamin L. Elsworth, Sunny Z. Wu, Daniel Roden, et al.
Nature Communications, 2018
The role of the extracellular matrix and its molecular and cellular regulators in cancer cell plasticity
Valentina Poltavets, Marina Kochetkova, Stuart M. Pitson, Michael S. Samuel
Frontiers in Oncology, 2018
Role of the β common (βc) family of cytokines in health and disease
Timothy R. Hercus, Winnie L. T. Kan, Sophie E. Broughton, Denis Tvorogov, Hayley S. Ramshaw, et al.
Cold Spring Harbor Perspectives in Biology, 2018
Wound Healing and the Non-cellular Microenvironment
Hayley S. Ramshaw, Jasreen Kular, Michael S. Samuel
Wound Healing Stem Cells Repair and Restorations Basic and Clinical Aspects, 2018
Rho–ROCK signaling regulates tumor-microenvironment interactions
Mohammad Zahied Johan, Michael S. Samuel
Biochemical Society Transactions, 2018
A RhoA-FRET Biosensor Mouse for Intravital Imaging in Normal Tissue Homeostasis and Disease Contexts
Max Nobis, David Herrmann, Sean C. Warren, Shereen Kadir, Wilfred Leung, et al.
Cell Reports, 2017
Transient tissue priming via ROCK inhibition uncouples pancreatic cancer progression, sensitivity to chemotherapy, and metastasis
Claire Vennin, Venessa T. Chin, Sean C. Warren, Morghan C. Lucas, David Herrmann, et al.
Science Translational Medicine, 2017
Epidermal YAP2-5SA-ΔC Drives β-Catenin Activation to Promote Keratinocyte Proliferation in Mouse Skin In Vivo
Bassem Akladios, Veronica Mendoza-Reinoso, Michael S. Samuel, Edna C. Hardeman, Kiarash Khosrotehrani, et al.
Journal of Investigative Dermatology, 2017
ROCK signaling promotes collagen remodeling to facilitate invasive pancreatic ductal adenocarcinoma tumor cell growth
Nicola Rath, Jennifer P Morton, Linda Julian, Lena Helbig, Shereen Kadir, et al.
EMBO Molecular Medicine, 2017
Tissue-selective expression of a conditionally-active ROCK2-estrogen receptor fusion protein
Michael S. Samuel, Nicola Rath, Siti F. Masre, Sarah T. Boyle, David A. Greenhalgh, et al.
Genesis, 2016
Mechano-reciprocity is maintained between physiological boundaries by tuning signal flux through the Rho-associated protein kinase
Sarah T. Boyle, Michael S. Samuel
Small Gtpases, 2016
The 7th Barossa Meeting--Cell Signalling in Cancer Biology and Therapy in Barossa Valley, Australia
M A Grimbaldeston, V M Dixit, M S Samuel
Cell Death Disease, 2016
An oncogenic role for sphingosine kinase 2
Heidi A. Neubauer, Duyen H. Pham, Julia R. Zebol, Paul A.B. Moretti, Amanda L. Peterson, et al.
Oncotarget, 2016
A Negative Regulatory Mechanism Involving 14-3-3ζ Limits Signaling Downstream of ROCK to Regulate Tissue Stiffness in Epidermal Homeostasis
Jasreen Kular, Kaitlin G. Scheer, Natasha T. Pyne, Amr H. Allam, Anthony N. Pollard, et al.
Developmental Cell, 2015
Destabilisation of dimeric 14-3-3 proteins as a novel approach to anti-cancer therapeutics
Joanna M. Woodcock, Carl Coolen, Katy L. Goodwin, Dong Jae Baek, Robert Bittman, et al.
Oncotarget, 2015
Cytoskeletal protein Flightless I inhibits apoptosis, enhances tumor cell invasion and promotes cutaneous squamous cell carcinoma progression
Zlatko Kopecki, Gink N. Yang, Jessica E. Jackson, Elizabeth L. Melville, Matthew P. Caley, et al.
Oncotarget, 2015
Interleukin-3-mediated regulation of β-catenin in myeloid transformation and acute myeloid leukemia
Teresa Sadras, Michelle Perugini, Chung H Kok, Diana G Iarossi, Susan L Heatley, et al.
Journal of Leukocyte Biology, 2014
Mechanisms of vitamin D3 metabolite repression of IgE-dependent mast cell activation
Kwok-Ho Yip, Natasha Kolesnikoff, Chunping Yu, Nicholas Hauschild, Houng Taing, et al.
Journal of Allergy and Clinical Immunology, 2014
Mechanotransduction pathways promoting tumor progression are activated in invasive human squamous cell carcinoma
S. Jan Ibbetson, Natasha T. Pyne, Anthony N. Pollard, Michael F. Olson, Michael S. Samuel
American Journal of Pathology, 2013
Tropomyosin regulates cell migration during skin wound healing
Justin G. Lees, Yu Wooi Ching, Damian H. Adams, Cuc T.T. Bach, Michael S. Samuel, et al.
Journal of Investigative Dermatology, 2013
Inhibition of CXCR2 profoundly suppresses inflammation-driven and spontaneous tumorigenesis
Thomas Jamieson, Mairi Clarke, Colin W. Steele, Michael S. Samuel, Jens Neumann, et al.
Journal of Clinical Investigation, 2012
Actomyosin contractililty: Force power drives tumor growth
Michael S. Samuel, Michael F. Olson
Cell Cycle, 2011
p53-mediated transcriptional regulation and activation of the actin cytoskeleton regulatory RhoC to LIMK2 signaling pathway promotes cell survival
Daniel R Croft, Diane Crighton, Michael S Samuel, Filipe C Lourenco, June Munro, et al.
Cell Research, 2011
K-Ras mediated murine epidermal tumorigenesis is dependent upon and associated with elevated Rac1 activity
Michael S. Samuel, Filipe C. Lourenço, Michael F. Olson
Plos One, 2011
Actomyosin-mediated cellular tension drives increased tissue stiffness and β-catenin activation to induce epidermal hyperplasia and tumor growth
Michael S. Samuel, Jose I. Lopez, Ewan J. McGhee, Daniel R. Croft, David Strachan, et al.
Cancer Cell, 2011
The Rho-regulated ROCK kinases in cancer
Grant R Wickman, Michael S. Samuel, Pamela A Lochhead, Michael F Olson
Rho Gtpases in Cancer, 2010
Dying alone: A tale of Rho
Michael S. Samuel, Michael F. Olson
Cell Stem Cell, 2010
Genetic dissection of differential signaling threshold requirements for the Wnt/β-catenin pathway in vivo
Michael Buchert, Dimitris Athineos, Helen E. Abud, Zoe D. Burke, Maree C. Faux, et al.
Plos Genetics, 2010
Tissue selective expression of conditionally-regulated ROCK by gene targeting to a defined locus
Michael S. Samuel, June Munro, Sheila Bryson, Stephen Forrow, David Stevenson, et al.
Genesis, 2009
Elevated Dnmt3a Activity Promotes Polyposis in ApcMin Mice by Relaxing Extracellular Restraints on Wnt Signaling
Michael S. Samuel, Hiromu Suzuki, Michael Buchert, Tracy L. Putoczki, Niall C. Tebbutt, et al.
Gastroenterology, 2009
Identification of putative targets of DNA (cytosine-5) methylationmediated transcriptional silencing using a novel conditionally active form of DNA methyltransferase 3a
Michael S. Samuel, Michael S. Samuel, Therèse Lundgren-May, Matthias Ernst
Growth Factors, 2007
DNA-methylation-dependent alterations of claudin-4 expression in human bladder carcinoma
Stéphanie Boireau, Michael Buchert, Michael S. Samuel, Julie Pannequin, Joanne L. Ryan, et al.
Carcinogenesis, 2007
Forced dimerization of gp130 leads to constitutive STAT3 activation, cytokine-independent growth, and blockade of differentiation of embryonic stem cells
Christiane Stuhlmann-Laeisz, Sigrid Lang, Athena Chalaris, Paliga Krzysztof, Sudarman Enge, et al.
Molecular Biology of the Cell, 2006
Role of the Escherichia coli glgX gene in glycogen metabolism
David Dauvillée, Isabelle S. Kinderf, Zhongyi Li, Behjat Kosar-Hashemi, Michael S. Samuel, et al.
Journal of Bacteriology, 2005
Barley sex6 mutants lack starch synthase lla activity and contain a starch with novel properties
Matthew K. Morell, Behjat Kosar‐Hashemi, Mark Cmiel, Michael S. Samuel, Peter Chandler, et al.
Plant Journal, 2003
Biochemical characterization of the Chlamydomonas reinhardtii α-1,4 glucanotransferase supports a direct function in amylopectin biosynthesis
Christophe Colleoni, David Dauvillée, Gregory Mouille, Matthew Morell, Michael Samuel, et al.
Plant Physiology, 1999
Novel, starch-like polysaccharides are synthesized by an unbound form of granule-bound starch synthase in glycogen-accumulating mutants of Chlamydomonas reinhardtii
David Dauvillée, Christophe Colleoni, Eudean Shaw, Gregory Mouille, Christophe D'Hulst, et al.
Plant Physiology, 1999
Genetic and biochemical evidence for the involvement of α-1,4 glucanotransferases in amylopectin synthesis
Christophe Colleoni, David Dauvillée, Gregory Mouille, Alain Buléon, Daniel Gallant, et al.
Plant Physiology, 1999
Fluorophore-assisted carbohydrate electrophoresis (FACE) of oligosaccharides: Efficiency of labelling and high-resolution separation
Michael G. O’Shea, Michael S. Samuel, Christine M. Konik, Matthew K. Morell
Carbohydrate Research, 1998
Analysis of starch structure using fluorophore-assisted carbohydrate electrophoresis
Mathew K. Morell, Michael S. Samuel, Michael G. O'Shea
Electrophoresis, 1998
Erratum: A complex arrangement of genes at a starch branching enzyme I locus in the D-genome donor of wheat (Genome (1997) 40 (465-474))
S Rahman, S Abrahams, D Abbott, Y Mukai, M Samuel, et al.
Genome, 1998
Differential expression and properties of starch branching enzyme isoforms in developing wheat endosperm
M. K. Morell, A. Blennow, B. Kosar-Hashemi, M. S. Samuel
Plant Physiology, 1997
A complex arrangement of genes at a starch branching enzyme I locus in the D-genome donor of wheat
S. Rahman, M. Morell, R. Appels, S. Abrahams, D. Abbott, et al.
Genome, 1997
The major proteins of wheat endosperm starch granules
S Rahman, B Kosar-Hashemi, MS Samuel, A Hill, DC Abbott, et al.
Australian Journal of Plant Physiology, 1995

Michael Susithiran Samuel

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