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the faster migrating Tg adduct C primarily engages the CaBP1 (Montrer S100G Kits ELISA)/P5 oxidoreductase (Montrer TXNRD1 Kits ELISA), whereas the slower migrating Tg adduct A primarily engages ERp72 (Montrer PDIA4 Kits ELISA).
Present the NMR structure of full-length CaBP1 (Montrer S100G Kits ELISA) with Ca(2 (Montrer CA2 Kits ELISA)+) bound at the first, third, and fourth EF-hands.
Different kinetics of Ca-dependent binding step between caldendrin and calmodulin (Montrer CALM1 Kits ELISA) with AKAP79 (Montrer AKAP5 Kits ELISA) suggest their different roles in synaptic function.
We demonstrate that calmodulin (Montrer CALM1 Kits ELISA) and caldendrin compete for a partially overlapping binding site on AKAP79 (Montrer AKAP5 Kits ELISA) and that their binding is differentially dependent on calcium
CaBP1 (Montrer S100G Kits ELISA) regulates voltage-dependent inactivation and activation of Ca(V)1.2 (Montrer CACNA1C Kits ELISA) (L-type) calcium channels
Structural basis for the differential effects of CaBP1 (Montrer S100G Kits ELISA) and calmodulin (Montrer CALM1 Kits ELISA) on Ca(V)1.2 (Montrer CACNA1C Kits ELISA) calcium-dependent inactivation.
enhances inactivation, causes a depolarizing shift in the voltage dependence of activation, and does not support Ca2 (Montrer CA2 Kits ELISA)+-dependent facilitation of Ca(v)2.1 (Montrer CACNA1A Kits ELISA) channels
CaBP1 (Montrer S100G Kits ELISA) is able to specifically regulate InsP3 receptor-mediated alterations in [Ca2 (Montrer CA2 Kits ELISA)+]i during agonist stimulation.
We describe a new role for CaBP1 (Montrer S100G Kits ELISA) in regulation of Ca2 (Montrer CA2 Kits ELISA)+ influx through Ca(v)1.2 (Montrer CACNA1C Kits ELISA) (L-type) Ca2 (Montrer CA2 Kits ELISA)+ channels. CaBP1 (Montrer S100G Kits ELISA) interacts directly with the alpha1 subunit of Ca(v)1.2 (Montrer CACNA1C Kits ELISA) at sites that also bind Calmodulin (Montrer CALM1 Kits ELISA)
the NT and IQ-domains of alpha(1)1.2 mediate functionally distinct interactions with CaBP1 (Montrer S100G Kits ELISA) and CaM (Montrer CALM1 Kits ELISA) that promote conformational alterations that either stabilize or inhibit inactivation of Ca(v)1.2 (Montrer CACNA1C Kits ELISA).
Results show that CaBP1/caldendrin and CaBP2 (Montrer CABP2 Kits ELISA) are not required for normal gross retinal and synapse morphology but are necessary for the proper transmission of light responses through the retina; CaBP1/caldendrin and CaBP2 (Montrer CABP2 Kits ELISA) likely act by modulating presynaptic Ca(2 (Montrer CA2 Kits ELISA)+)-dependent signaling mechanisms.
Study provides the first report of the expression and localization of CaBP1 and caldendrin in the mouse brain
These findings suggest that expression of paracellular tight junction genes is regulated by transcellular CaBP (Montrer S100G Kits ELISA) proteins, suggesting that active and passive calcium transport pathways may function cooperatively
TRPV6 (Montrer TRPV6 Kits ELISA), NCX1 (Montrer SLC8A1 Kits ELISA), and CaBP (Montrer S100G Kits ELISA)-9k in the fetal placenta and CaBP (Montrer S100G Kits ELISA)-28k in the maternal placenta may play key roles in controlling calcium transport across the placenta during pregnancy.
When immature mice were treated with 17beta-estradiol or progesterone for 3 days, we found that the expressions of Bax (Montrer BAX Kits ELISA) and caspase 3 protein (Montrer CASP3 Kits ELISA) were increased by estradiol treatment in WT and CaBP (Montrer S100G Kits ELISA)-9k KO mice.
our results implicate CaBP1 rather than CaBP4 (Montrer CABP4 Kits ELISA) in conferring the anomalous slow inactivation of Ca(v)1.3 (Montrer CACNA1D Kits ELISA) Ca(2 (Montrer CA2 Kits ELISA)+) currents required for auditory transmission
Regulation of calbindin-D9k (Montrer S100G Kits ELISA) expression by 1,25-dihydroxyvitamin D(3) and parathyroid hormone (Montrer PTH Kits ELISA) in mouse primary renal tubular cells
These results suggest that the mouse uterine calbindin-D9k (Montrer S100G Kits ELISA) gene is expressed under the control of a progesterone response element.
demonstrated that the CaBP (Montrer S100G Kits ELISA)-9k is distinctly regulated in the mouse placenta and extra-embryonic membrane, probably via sex steroid hormones (E2 and P4) and their receptors through a complex pathway
Progesterone and its receptor may be dominant factors in the regulation of CaBP (Montrer S100G Kits ELISA)-9k but estrogen and ERalpha (Montrer ESR1 Kits ELISA) can influence the expression of the CaBP (Montrer S100G Kits ELISA)-9k gene via an indirect pathway in the uterus of immature mice.
Calcium binding proteins are an important component of calcium mediated cellular signal transduction. This gene encodes a protein that belongs to a subfamily of calcium binding proteins which share similarity to calmodulin. The protein encoded by this gene regulates the gating of voltage-gated calcium ion channels. This protein inhibits calcium-dependent inactivation and supports calcium-dependent facilitation of ion channels containing voltage-dependent L-type calcium channel subunit alpha-1C. This protein also regulates calcium-dependent activity of inositol 1,4,5-triphosphate receptors, P/Q-type voltage-gated calcium channels, and transient receptor potential channel TRPC5. This gene is predominantly expressed in retina and brain. Alternative splicing results in multiple transcript variants encoding disinct isoforms.
, calcium-binding protein 1
, calcium binding protein 1
, calcium binding protein 5
, calcium binding protein 1 (calbrain)
, S100 calcium-binding protein G
, calbindin 3, (vitamin D-dependent calcium binding protein)
, calbindin D9k
, calbindin-D9K major form
, cytidine 5'-triphosphate synthase 2
, protein S100-G
, vitamin D-dependent calcium-binding protein, intestinal