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1 in mice lacking the calcium-binding protein calbindin D28k.
2 irus overexpressing the Ca2+ binding protein calbindin D28k.
3 f conformational change between apo and holo calbindin-D28k.
4 rons also immunolabeled with the antibody to calbindin-D28k.
5 CL and express the neuronal markers NeuN and calbindin-D28k.
6 expressing neurones were found to co-express calbindin D28k (36%), the glutamate transporter EAAC-1 (
10 used several histochemical stains, including calbindin-D28k, a marker of the shell compartment, acety
11 , revealed a striking correspondence between calbindin D28k and huntingtin immunoreactivities, with l
12 e the exact calcium-binding stoichiometry of calbindin D28K and two mutant forms of the protein, one
13 ndin-D28K cDNA-infected cells expressed high calbindin-D28K and demonstrated increased resistance to
15 transferase, SPR/somatostatin, SPR/GABA, SPR/calbindin D28k, and SPR/parvalbumin double immunolabelin
16 ned genetic disruption of parvalbumin-alpha, calbindin-D28k, and calretinin in mice with patch-clamp
17 to the neuronal markers NeuN, glutamate, and calbindin-D28k, and to receptors for fibroblast growth f
21 cells containing the calcium-binding protein calbindin-D28K (CaBP), sustained circadian locomotor rhy
22 ontain nonpyramidal cells immunoreactive for calbindin-D28K (CALB), parvalbumin (PARV), and calretini
24 physiological experiments, in which purified calbindin-D28k (calbindin) and calretinin antibodies wer
25 f gamma-aminobutyric acidergic interneurons (calbindin-D28k, calretinin, parvalbumin) in 13 HD cases
27 us monkey, we found that the distribution of calbindin D28K (CB) and parvalbumin (PV) is nonoverlappi
28 lcium-binding proteins parvalbumin (PVB) and calbindin D28k (CB) are coexpressed in large subpopulati
30 ding ratio (kappa) after complete washout of calbindin D28k (Cb), kappafixed, displayed a substantial
31 atiotemporal analysis of the localization of calbindin-D28k (CB) and calretinin (CR) immunoreactive s
32 reased levels of the calcium-binding protein calbindin-D28k (CB) and the calcium-dependent immediate
33 calcium-binding proteins calretinin (CR) and calbindin-D28k (CB) have been widely used to characteriz
35 s to vasoactive intestinal peptide (VIP) and calbindin-D28K (CB) labeled two separate interneuronal s
36 teins calretinin (CR), parvalbumin (PV), and calbindin-D28k (CB) to characterize the gecko auditory s
37 of three cytosolic calcium-binding proteins: calbindin-D28k (CB), calretinin (CR), and parvalbumin (P
38 alization with the calcium-binding proteins; calbindin-D28k (CB), parvalbumin (PV), and calretinin (C
39 lls were infected with a retrovirus carrying calbindin-D28K cDNA under the control of the promoter of
41 xynucleotides, which significantly decreased calbindin-D28K expression, rendered these cells vulnerab
43 solution structure of disulfide-reduced holo-calbindin-D28k has been determined by NMR, while the str
45 traced for up to 413 microm from the soma in calbindin D28k-identified Renshaw cells and up to 184 mi
46 ssential tremor and 39 control brains, using calbindin D28k immunohistochemistry on 100-microm cerebe
47 s serial sections stained for enkephalin and calbindin D28k immunoreactivities showed that the topogr
48 pinal cord by their morphology, location and calbindin D28K immunoreactivity, were present at 11 week
49 A combination of anti-gephyrin- and anti-calbindin D28k-immunoreactivity was used to identify 129
50 rescence for either nitric oxide synthase or calbindin D28k in comparison with huntingtin expression,
51 s mutant PS1 and the calcium binding protein calbindin-D28k in ECL2 are also susceptible to lesion-in
53 ntibody against the calcium-binding protein, calbindin-D28K, in normal autopsy tissue and the neurona
54 tigen, microtubule-associated protein-2, and calbindin D28k, indicating that the newly divided cells
63 The major calcium buffer in these cells, calbindin D28K, is present only after differentiation ha
64 controlled by a native fast calcium buffer, calbindin-D28k, maintaining a lower vesicular release pr
65 atal systems expressing immunoreactivity for calbindin D28k, met-enkephalin, substance P, tyrosine hy
66 of the intracellular Ca2+-buffering proteins calbindin-D28k or parvalbumin, exclude the possibility t
67 tive label), FG retrograde label, and either calbindin-D28k or synaptophysin immunohistochemistry.
68 label experiments, 5-HT2A label was found in calbindin D28k-positive, nonphosphorylated-neurofilament
69 immunocytochemistry revealed m1 receptors in calbindin-D28k--positive medium spiny projection neurons
70 verexpression of the calcium-binding protein calbindin D28k prevents apoptosis in cultured neural cel
71 abelling with antibodies against gephyrin or calbindin D28k to provide immunohistochemical identifica
72 lar sections were stained with antibodies to calbindin-D28k (to visualize Purkinje cells) and vesicul
73 for the first time, the specific regions of calbindin-D28k undergoing conformational changes between
74 gene transfer of the calcium-binding protein calbindin D28k via a Herpes simplex amplicon vector decr
75 ole for calbindin-D28k in the beta cell, rat calbindin-D28k was overexpressed in the pancreatic beta
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