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抗Human CABP1 抗体:
抗Mouse (Murine) CABP1 抗体:
抗Rat (Rattus) CABP1 抗体:
Human Polyclonal CABP1 Primary Antibody for ELISA, WB - ABIN249625
Yamaguchi, Yamaguchi, Miyamoto, Sugimoto, Konishi, Hatase, Tokuda: Calbrain, a novel two EF-hand calcium-binding protein that suppresses Ca2+/calmodulin-dependent protein kinase II activity in the brain. in The Journal of biological chemistry 1999
the faster migrating Tg adduct C primarily engages the CaBP1 (显示 S100G 抗体)/P5 oxidoreductase (显示 TXNRD1 抗体), whereas the slower migrating Tg adduct A primarily engages ERp72 (显示 PDIA4 抗体).
Present the NMR structure of full-length CaBP1 (显示 S100G 抗体) with Ca(2 (显示 CA2 抗体)+) bound at the first, third, and fourth EF-hands.
Different kinetics of Ca-dependent binding step between caldendrin and calmodulin (显示 CALM1 抗体) with AKAP79 (显示 AKAP5 抗体) suggest their different roles in synaptic function.
We demonstrate that calmodulin (显示 CALM1 抗体) and caldendrin compete for a partially overlapping binding site on AKAP79 (显示 AKAP5 抗体) and that their binding is differentially dependent on calcium
CaBP1 (显示 S100G 抗体) regulates voltage-dependent inactivation and activation of Ca(V)1.2 (显示 CACNA1C 抗体) (L-type) calcium channels
Structural basis for the differential effects of CaBP1 (显示 S100G 抗体) and calmodulin (显示 CALM1 抗体) on Ca(V)1.2 (显示 CACNA1C 抗体) calcium-dependent inactivation.
enhances inactivation, causes a depolarizing shift in the voltage dependence of activation, and does not support Ca2 (显示 CA2 抗体)+-dependent facilitation of Ca(v)2.1 (显示 CACNA1A 抗体) channels
CaBP1 (显示 S100G 抗体) is able to specifically regulate InsP3 receptor-mediated alterations in [Ca2 (显示 CA2 抗体)+]i during agonist stimulation.
We describe a new role for CaBP1 (显示 S100G 抗体) in regulation of Ca2 (显示 CA2 抗体)+ influx through Ca(v)1.2 (显示 CACNA1C 抗体) (L-type) Ca2 (显示 CA2 抗体)+ channels. CaBP1 (显示 S100G 抗体) interacts directly with the alpha1 subunit of Ca(v)1.2 (显示 CACNA1C 抗体) at sites that also bind Calmodulin (显示 CALM1 抗体)
the NT and IQ-domains of alpha(1)1.2 mediate functionally distinct interactions with CaBP1 (显示 S100G 抗体) and CaM (显示 CALM1 抗体) that promote conformational alterations that either stabilize or inhibit inactivation of Ca(v)1.2 (显示 CACNA1C 抗体).
Results show that CaBP1/caldendrin and CaBP2 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 likely act by modulating presynaptic Ca(2 (显示 CA2 抗体)+)-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 (显示 S100G 抗体) proteins, suggesting that active and passive calcium transport pathways may function cooperatively
TRPV6 (显示 TRPV6 抗体), NCX1 (显示 SLC8A1 抗体), and CaBP (显示 S100G 抗体)-9k in the fetal placenta and CaBP (显示 S100G 抗体)-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 (显示 BAX 抗体) and caspase 3 protein (显示 CASP3 抗体) were increased by estradiol treatment in WT and CaBP (显示 S100G 抗体)-9k KO mice.
Regulation of calbindin-D9k (显示 S100G 抗体) expression by 1,25-dihydroxyvitamin D(3) and parathyroid hormone (显示 PTH 抗体) in mouse primary renal tubular cells
These results suggest that the mouse uterine calbindin-D9k (显示 S100G 抗体) gene is expressed under the control of a progesterone response element.
demonstrated that the CaBP (显示 S100G 抗体)-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 (显示 S100G 抗体)-9k but estrogen and ERalpha (显示 ESR1 抗体) can influence the expression of the CaBP (显示 S100G 抗体)-9k gene via an indirect pathway in the uterus of immature mice.
These results suggest that calcium regulates CaBP-D9k expression by modulating the circulating 1,25-dihydrxyvitamin D(3) level and that Vitamin D receptor (显示 VDR 抗体) is thus required for the dietary calcium-induced suppression of CaBP-D9k expression.
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