Results 91 to 100 of about 41,736 (257)

Single-channel recording of inositol trisphosphate receptor in the isolated nucleus of a muscle cell line

open access: yesBiological Research, 2006
Nuclear calcium appears to have an important role in the regulation of gene expression in many cells, but the mechanisms involved in controlling nuclear Ca2+ signaling are controversial and still poorly understood.
CARLOS KUSNIER   +3 more
doaj  

A New Case of Lethal Congenital Contracture Syndrome Type 3 With Hyperinsulinism and Optic Atrophy

open access: yesClinical Genetics, EarlyView.
PIP5K1C‐related lethal congenital contracture syndrome with hyperinsulinism and optic atrophy. ABSTRACT Lethal congenital contracture syndrome 3 (LCCS3, MIM #611369) is a rare autosomal recessive neuromuscular disorder caused by biallelic loss‐of‐function (LOF) variants in PIP5K1C, reported in only two families to date.
Tameemi Abdalla Moady   +3 more
wiley   +1 more source

The dynamics of the IP3 model .

open access: yes, 2013
The dynamics of the IP3 model .
Claudine Chaouiya (242549)   +2 more
core   +1 more source

Antipsychotics‐Induced Hyposalivation Mediated by Impaired Salivary Ca2+ Signaling

open access: yesOral Diseases, EarlyView.
ABSTRACT Objectives Antipsychotic‐induced salivary dysfunction such as hyposalivation is a prevalent clinical challenge that severely compromises oral health and quality of life. Although typical and atypical antipsychotics have their therapeutic target in the central nervous system, their direct molecular mechanisms within the salivary glands remain ...
Chaelin Chung   +4 more
wiley   +1 more source

Synthesis and characterization of cell-permeant 6-nitrodibenzofuranyl-caged IP3

open access: yes, 2012
We have synthesized in a 6-nitrodibenzofuranyl (NDBF) derivative of inositol-1,4,5-trisphosphate (IP3) for efficient two-photon uncaging in living cells.
Kantevari, Srinivas   +5 more
core   +1 more source

Structural insights into the regulatory mechanism of IP3 receptor [PDF]

open access: yes, 2004
Inositol 1,4,5-trisphosphate receptors (IP3R) are intracellular Ca2+ release channels whose opening requires binding of two intracellular messengers IP3 and Ca2+.
Mitsuhiko Ikura   +7 more
core   +1 more source

Ion Channel Dysfunction and Therapeutic Targeting in Salivary Gland Disorders

open access: yesOral Diseases, EarlyView.
ABSTRACT Objective Salivary gland hypofunction and xerostomia represent major clinical complications of radiation therapy, autoimmune disorders such as Sjögren's disease, and inherited epithelial ion transport defects. This review integrates current knowledge on ion channel dysfunction as a central mechanistic driver of salivary gland pathology and ...
Tarek Mohamed Abd El‐Aziz   +6 more
wiley   +1 more source

Synthetic partial agonists reveal key steps in IP3 receptor activation [PDF]

open access: yes, 2009
Inositol 1,4,5-trisphosphate receptors (IP3Rs) are ubiquitous intracellular Ca2+ channels. IP3 binding to the IP 3-binding core (IBC) near the N terminus initiates conformational changes that lead to opening of a pore.
Emily J A Taylor   +18 more
core   +1 more source

My Brief Encounter with the Phosphoinositides and IP3 [PDF]

open access: yesJournal of Biological Chemistry, 2004
. Before describing thisresearch, however, I should say how that choice came about. While in graduate school at theUniversity of Wisconsin, I had had the good fortune to study under Karl Paul Link, who waswidely renowned for his discovery of dicumarol and the synthesis of related blood anticoagu-lants such as warfarin, work that was recognized with two
openaire   +2 more sources

TMEM16A channel signalling microdomains in the regulation of vascular function

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Schematic representation of TMEM16A channel signalling microdomains. Calcium influx or calcium release from the endoplasmic/sarcoplasmic reticulum (ER/SR) activates TMEM16A channels through interactions with regulatory proteins in vascular smooth muscle cells or endothelial cells. TMEM16A channel activation drives chloride efflux,
Fênix Araujo, Swapnil K. Sonkusare
wiley   +1 more source

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