Marites T. Woon
University of Wisconsin-Madison
Protein subunitInduced pluripotent stem cellInternal medicineEndocrinologyPatch clampMolecular biologyMuscle hypertrophyHEK 293 cellsChemistryVoltage-dependent calcium channelMyocyteDilated cardiomyopathyCaveolin 3Cav1.2CardiomyopathyStem cellL type ca2 channelsIon channelMedicineBiologyCell biologyLeucine-rich repeat
11Publications
4H-index
63Citations
Publications 11
Newest
#1Mitch Biermann (UW: University of Wisconsin-Madison)H-Index: 4
#2Wenxuan Cai (UW: University of Wisconsin-Madison)H-Index: 15
Last. Timothy J. Kamp (UW: University of Wisconsin-Madison)H-Index: 56
view all 21 authors...
: Human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) exhibit a fetal phenotype that limits in vitro and therapeutic applications. Strategies to promote cardiomyocyte maturation have focused interventions on differentiated hPSC-CMs, but this study tests priming of early cardiac progenitor cells (CPCs) with polyinosinic-polycytidylic acid (pIC) to accelerate cardiomyocyte maturation. CPCs were differentiated from hPSCs using a monolayer differentiation protocol with defined small molecu...
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#1Leonid Tyan (UW: University of Wisconsin-Madison)H-Index: 11
#2Jason D. Foell (UW: University of Wisconsin-Madison)H-Index: 12
Last. Timothy J. Kamp (UW: University of Wisconsin-Madison)H-Index: 56
view all 12 authors...
KEY POINTS: Mutations in the caveolae scaffolding protein, caveolin-3 (Cav3), have been linked to the long QT type 9 inherited arrhythmia syndrome (LQT9) and the cause of underlying action potential duration prolongation is incompletely understood. In the present study, we show that LQT9 Cav3 mutations, F97C and S141R, cause mutation-specific gain of function effects on Cav 1.2-encoded L-type Ca2+ channels responsible for ICa,L and also cause loss of function effects on heterologously expressed ...
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#1Mitch BiermannH-Index: 4
#2Wenxuan CaiH-Index: 15
Last. Timothy J. KampH-Index: 56
view all 11 authors...
Cardiomyocytes derived from human induced pluripotent stem cells (hiPS-CMs) hold promise for disease modeling, drug discovery, and therapy, but the challenge remains to create mature cardiomyocytes...
#1Marites T. Woon (UW: University of Wisconsin-Madison)H-Index: 4
#2Pamela A. Long (Mayo Clinic)H-Index: 7
Last. Timothy J. Kamp (UW: University of Wisconsin-Madison)H-Index: 56
view all 11 authors...
BackgroundGenetic causes of dilated cardiomyopathy (DCM) are incompletely understood. LRRC10 (leucine‐rich repeat–containing 10) is a cardiac‐specific protein of unknown function. Heterozygous muta...
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#1Marites T. WoonH-Index: 4
#2Pamela A. LongH-Index: 7
Last. Timothy J. KampH-Index: 56
view all 11 authors...
Leucine-rich repeat containing (LRR) proteins facilitate protein-protein interactions critical in a number of cellular functions including ion channel regulation. Leucine-rich repeat containing pro...
#1Marites T. Woon (UW: University of Wisconsin-Madison)H-Index: 4
#2Timothy J. Kamp (UW: University of Wisconsin-Madison)H-Index: 56
Personalized heart muscle cells made from stem cells in the laboratory could be used to check an individual’s response to potential new drugs before clinical trials.
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#1Marites T. WoonH-Index: 4
Last. Timothy J. KampH-Index: 56
view all 10 authors...
Leucine-rich repeat containing protein 10 (LRRC10) is a cardiac-specific protein and loss of LRRC10 in LRRC10-/- mice results in dilated cardiomyopathy (DCM). Here we describe a novel mutation in h...
#1Yogananda S. Markandeya (UW: University of Wisconsin-Madison)H-Index: 10
#2Laura J. Phelan (UW: University of Wisconsin-Madison)H-Index: 1
Last. Ravi C. Balijepalli (UW: University of Wisconsin-Madison)H-Index: 22
view all 10 authors...
Abstract Pathological cardiac hypertrophy is characterized by subcellular remodeling of the ventricular myocyte with a reduction in the scaffolding protein caveolin-3 (Cav-3), altered Ca2+ cycling, increased protein kinase C expression, and hyperactivation of calcineurin/nuclear factor of activated T cell (NFAT) signaling. However, the precise role of Cav-3 in the regulation of local Ca2+ signaling in pathological cardiac hypertrophy is unclear. We used cardiac-specific Cav-3-overexpressing mice...
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#1Marites T. Woon (UW: University of Wisconsin-Madison)H-Index: 4
#2Ravi C. Balijepalli (UW: University of Wisconsin-Madison)H-Index: 22
Low voltage activated T-type calcium channels (TTCC) play a pivotal role in the developing heart. Although the TTCC isoforms, Cav3.1 and Cav3.2, underlie cardiac TTCC current (ICa,T) and are expressed in atrial and ventricular myocytes during development, their expression and roles recede in the adult heart. However, previous studies have demonstrated the re-expression of ICa,T in pathological cardiac hypertrophy, suggesting that TTCCs contribute to the altered Ca2+ cycling and signaling in thes...
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#1Marites T. Woon (UW: University of Wisconsin-Madison)H-Index: 4
#2Adrian C. Grimes (UW: University of Wisconsin-Madison)H-Index: 10
Last. Ravi C. Balijepalli (UW: University of Wisconsin-Madison)H-Index: 22
view all 6 authors...
Cardiac L-type Ca2+ channels (LTCC) play essential role in multiple cellular processes including excitation-contraction coupling, signaling and gene regulation. Diverse families of regulatory and scaffolding proteins regulate the LTCCs in the cardiomyocytes. Leucine-rich repeat containing 10 (LRRC10) is a cardiac-specific scaffolding protein that plays a critical role in heart development and function. Recently we have demonstrated that the Lrrc10-null (Lrrc10-/-) mice develop dilated cardiomyop...
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