W
William D. Swaim
Researcher at National Institutes of Health
Publications - 66
Citations - 3829
William D. Swaim is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Salivary gland & Submandibular gland. The author has an hindex of 33, co-authored 65 publications receiving 3493 citations.
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Journal ArticleDOI
Matriptase/MT-SP1 is required for postnatal survival, epidermal barrier function, hair follicle development, and thymic homeostasis.
Karin List,Christian C. Haudenschild,Roman Szabo,Wanjun Chen,Sharon M. Wahl,William D. Swaim,Lars H. Engelholm,Lars H. Engelholm,Niels Behrendt,Thomas H. Bugge +9 more
TL;DR: It is demonstrated that Matriptase/MT-SP1 has pleiotropic functions in the development of the epidermis, hair follicles, and cellular immune system.
Journal ArticleDOI
α-Galactosidase A deficient mice: A model of Fabry disease
Toshio Ohshima,Gary J. Murray,William D. Swaim,Glenn Longenecker,Jane M. Quirk,Carol O. Cardarelli,Yoshikazu Sugimoto,Ira Pastan,Michael M. Gottesman,Roscoe O. Brady,Ashok B. Kulkarni +10 more
TL;DR: The similarity of the pathophysiological process in the mutant mice and in patients with Fabry disease is indicated, indicating the importance of an animal model for exploring therapeutic strategies for patients withFabry disease.
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Local Ca2+ Entry Via Orai1 Regulates Plasma Membrane Recruitment of TRPC1 and Controls Cytosolic Ca2+ Signals Required for Specific Cell Functions
TL;DR: It is suggested that coordinated regulation of the surface expression of TRPC1 by Orai1 and gating by STIM1 provides a mechanism for rapidly modulating and maintaining SOCE-generated Ca²+ signals.
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An alternative interpretation of nanobacteria-induced biomineralization
TL;DR: Evidence is provided that biomineralization previously attributed to nanobacteria may be initiated by nonliving macromolecules and transferred on "subculture" by self-propagating microcrystalline apatite.
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Attenuation of store-operated Ca2+ current impairs salivary gland fluid secretion in TRPC1(−/−) mice
Xibao Liu,Kwong Tai Cheng,Bidhan C. Bandyopadhyay,Biswaranjan Pani,Alexander Dietrich,Biman C. Paria,William D. Swaim,David J. Beech,Eda Yildrim,Brij B. Singh,Lutz Birnbaumer,Indu S. Ambudkar +11 more
TL;DR: It is reported that attenuation of SOC current underlies salivary gland dysfunction in mice lacking transient receptor potential 1 (TRPC1), and TRPC1 is a critical component of the SOC channel in salivARY gland acinar cells and is essential for neurotransmitter-regulation of fluid secretion.