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Junctional complexes between the plasma membrane and endoplasmic/sarcoplasmic reticulum are a common feature of all excitable cell types and mediate cross talk between cell surface and intracellular ion channels. Zusätzlich bieten wir Ihnen Junctophilin 2 Proteine (6) und viele weitere Produktgruppen zu diesem Protein an.
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Junctophilin-2 is cleaved by calpain at multiple sites, resulting in dysfunctional junctophilin-2 truncations.
Our data identify a mechanistic link between microtubule densification and T-tubule remodeling and reveal microtubule-mediated JP2 redistribution as a novel mechanism for T-tubule disruption, loss of excitation-contraction coupling, and heart failure.
The S101R mutation may have an effect upon the stability of the JP2 dyad organization with the potential to alter JP2-protein interactions regulating calcium cycling.
This study demonstrates that both JP1 (zeige JPH1 Antikörper) and JP2 in skeletal muscle undergo Ca2 (zeige CA2 Antikörper)+-dependent proteolysis by endogenous proteases when the intracellular Ca2 (zeige CA2 Antikörper)+ is raised within the physiological range for a sustained period
Hypertrophy in skeletal myotubes induced by junctophilin-2 mutant, Y141H, involves an increase in store-operated Ca2 (zeige CA2 Antikörper)+ entry via Orai1 (zeige ORAI1 Antikörper).
JP1 (zeige JPH1 Antikörper) and JP2 can facilitate the assembly of DHPR (zeige QDPR Antikörper) with other proteins of the excitation-contraction coupling machinery
Loss-of-function mutations in JPH2 leads to cardiac-specific JPH2 deficiency and results in impaired cardiac contractility, causing heart failure and increased mortality.
JPH2 levels are reduced in patients with hypertrophic cardiomyopathy. Reduced JPH2 expression results in reduced excitation-contraction coupling gain as well as altered Ca(2 (zeige CA2 Antikörper)+) homeostasis, which may be associated with prohypertrophic remodeling.
S165F mutation of junctophilin 2 affects Ca2 (zeige CA2 Antikörper)+ signalling in skeletal muscle.
this is the first report on JPH2 mutation associated with hypertrophic cardiomyopathy
A 3-fold increase in the junctophilin-2 to RyR2 (zeige RYR2 Antikörper) ratio is compatible with direct inhibition of RyR2 (zeige RYR2 Antikörper) opening by junctophilin-2 to intrinsically stabilize the Ca2 (zeige CA2 Antikörper)+ signaling properties of the junction and thus the contractile function of the cell.
This molecular rearrangement is compatible with direct inhibition of RyR (zeige RYR1 Antikörper) opening by junctophilin-2 to intrinsically stabilise the Ca(2 (zeige CA2 Antikörper)+) signalling properties of the junction and thus the contractile function of the cell.
These results suggested that NCX1 (zeige SLC8A1 Antikörper) may play an important role in the proper spatial distribution of LTCC and JP2 in T-tubules in the context of pressure-overloading.
overexpression of JP2 provided significantly protective benefits after pressure overload
JPH2 may be critical in anchoring the invaginating sarcolemma to the sarcoplasmic reticulum, thereby enabling the maturation of the transverse tubules network
JP2 deficiency abolished the increase in the density of transverse elements
Our data suggest a novel mechanism by which reduced JPH2-mediated stabilization of RyR2 (zeige RYR2 Antikörper) due to loss-of-function mutation or reduced JPH2/RyR2 (zeige RYR2 Antikörper) ratios can promote SR Ca(2 (zeige CA2 Antikörper)+) leak and atrial arrhythmias
Junctional complexes between the plasma membrane and endoplasmic/sarcoplasmic reticulum are a common feature of all excitable cell types and mediate cross talk between cell surface and intracellular ion channels. The protein encoded by this gene is a component of junctional complexes and is composed of a C-terminal hydrophobic segment spanning the endoplasmic/sarcoplasmic reticulum membrane and a remaining cytoplasmic domain that shows specific affinity for the plasma membrane. This gene is a member of the junctophilin gene family. Alternative splicing has been observed at this locus and two variants encoding distinct isoforms are described.
, junctophilin type 2