ライフサイエンスコーパス: CaBP

1 CaBP/caldendrin, a subfamily of the EF-hand-containing n

2 CaBPs display a restricted pattern of expression in neur

3 r the calcium binding protein calbindin-28K (CaBP) was used to identify the CaBP-poor sensorimotor an

4 Parvalbumin (PV), a CaBP with slow Ca(2+)-binding kinetics, shortened the du

5 In addition, CaBP immunocytochemistry, which correlates highly with e

6 d to undifferentiated Rcho-1 stem cells, and CaBP expression is upregulated.

7 Calbindin (CaBP)-D28k and CaBP-D9k are cytosolic vitamin D-dependent calcium-bindi

8 ts revealed very few neurons in which PV and CaBP immunoreactivities were colocalized.

9 e conclude that the distributions of PV+ and CaBP+ cell bodies in the raccoon somatosensory thalamus

10 The distributions of PV+ and CaBP+ cells tended to be complementary to each other in

11 ifferential pattern of PV-positive (PV+) and CaBP-positive (CaBP+) cells was found in the somatosenso

12 d to identify the CaBP-poor sensorimotor and CaBP-rich associative Str regions and the corresponding

13 The ability of Ca(2+) buffers and CaBPs with differing kinetics to fine-tune both global a

14 In reconstitution assays, CaBPs are able to substitute functionally for CaM.

15 ests that, in the rodent auditory brainstem, CaBP-containing cells do not express GAD67.

16 28k in calcium homeostasis is compensated by CaBP-D9k, we generated VDR/CaBP-D28k double knockout (KO

17 s calcemic role can be mostly compensated by CaBP-D9k.

18 minae in the SC that can be distinguished by CaBP content.

19 Calbindin (CaBP)-D28k and CaBP-D9k are cytosolic vitamin D-dependen

20 unoreactive for parvalbumin (PV), calbindin (CaBP), glutamic acid decarboxylase (GAD), and gamma-amin

21 transplants of half-SCN grafts that contain CaBP cells restore locomotor rhythms in SCN-lesioned hos

22 ontext in the known set of DxDxDG-containing CaBPs, including those where the structural resemblance

23 In contrast, CaBP+ neurons were distributed throughout VP, VPI, and P

24 ssociative Str regions and the corresponding CaBP-poor middle, CaBP-rich border, and the caudomedial

25 investigate the actions of mobile cytosolic CaBPs on the spatiotemporal properties of IP(3)-evoked C

26 , but also by expression of mobile cytosolic CaBPs under resting concentrations of IP(3).

27 the calcium-binding protein calbindin-D28K (CaBP), sustained circadian locomotor rhythms.

28 n an inducible manner and (2) downregulating CaBP expression using antisense technology, using the ra

29 on of GFRalpha-1-expressing neurons for each CaBP subpopulation indicated the coexistence of GFRalpha

30 stained with two different dilutions of each CaBP antibody used, revealed that 84% and 72% of the OT

31 Those cells stably expressing CaBP also exhibit higher levels of steady-state intracel

32 results also support a more direct role for CaBP in the trophoblast differentiation pathway.

33 how Co(2+) uptake and are immunopositive for CaBPs.

34 bindin D(28k), another member of the EF-hand CaBP superfamily.

35 arvalbumin family, relative to other EF-hand CaBPs in cochlear and vestibular organs in the mouse.

36 structure, and protein function for EF-hand CaBPs, as well as the additional mutations for the next

37 However, CaBPs are also expressed in the cell nucleus, suggesting

38 cium binding protein-28K immunoreactivities (CaBP; a marker for horizontal cells) were colocalized in

39 nal CaBP-D9k expression but little change in CaBP-D28k.

40 InsP(3), dependent on functional EF-hands in CaBP.

41 e than 40% of the pallidostriatal neurons in CaBP-poor middle GP region are PV-positive, whereas most

42 on are PV-positive, whereas most of those in CaBP-rich GP regions are PV-negative.

43 ions and the corresponding CaBP-poor middle, CaBP-rich border, and the caudomedial GP regions.

44 e cloning of a full-length cDNA of the mouse CaBP which shows significant homology with calreticulin,

45 Of multiple CaBPs detected in inner hair cells (CaBP1, CaBP2, CaBP4

46 In neurons, CaBPs are primarily localized to the cytosol and functio

47 acking, and the frequently used neuropeptide/CaBP signatures are subject to regulation by age and act

48 ouble knockout (KO) mice, which expressed no CaBP-D28k and only 10% of CaBP-D9k in the kidney.

49 These data suggest that these novel CaBPs are an important component of Ca(2+)-mediated cell

50 which expressed no CaBP-D28k and only 10% of CaBP-D9k in the kidney.

51 density of PV+ neurons had a low density of CaBP+ cell bodies.

52 Conversely, downregulation of CaBP expression had a negative effect on calcium uptake,

53 ver, the neuronally restricted expression of CaBP and its inhibition of InsP(3)R-mediated Ca(2+) sign

54 proteins (CaBP), apparently a major group of CaBP in bacteria.

55 astic giant cells supports the importance of CaBP in trophoblast maturation and the validity of the R

56 here was a correlation between the number of CaBP-positive cells in the graft and the strength of the

57 In addition, prolonged overexpression of CaBP in Rcho-1 cultures promotes trophoblast differentia

58 Our results show that overexpression of CaBP stimulates both cellular calcium uptake and vectori

59 The patterns of CaBP expression were complementary.

60 sport is likely to involve the regulation of CaBP expression to handle the increasing Ca requirements

61 To analyze the regulation of CaBP expression, placenta organ cultures and Rcho-1 cell

62 The functional role of CaBP in cellular Ca handling was investigated using a tr

63 study we have directly examined the role of CaBP in these processes by (1) recombinantly overexpress

64 To address whether the role of CaBP-D28k in calcium homeostasis is compensated by CaBP-

65 The upregulation of CaBP expression during and/or following the differentiat

66 eal unexpected diversity in the strengths of CaBPs as Ca(2+) channel modulators, and implicate CaBP1

67 rotein (PTHrP 1-34), and Ca had no effect on CaBP mRNA and protein levels, which were significantly s

68 sequence and structure of EhCaBP1 and other CaBPs indicates that the C-terminal domain of EhCaBP1 po

69 Recently, other CaBPs containing the same motif, but lacking one or both

70 rocesses by (1) recombinantly overexpressing CaBP in an inducible manner and (2) downregulating CaBP

71 tern of PV-positive (PV+) and CaBP-positive (CaBP+) cells was found in the somatosensory thalamus.

72 d according to their Ca(2+) binding protein (CaBP) content; thus, we also sought to investigate the p

73 identified a 57-kDa, Ca(2+)-binding protein (CaBP) functionally implicated in placental calcium trans

74 tr) projections and calcium binding protein (CaBP) immunostaining patterns of the Str and GP were use

75 find that CaM-like calcium-binding protein (CaBP) molecules are clearly expressed within the organ o

76 ecific, high M(r) 57-kDa Ca-binding protein (CaBP) plays an important role in regulating and/or shutt

77 valbumin, an EF-hand Ca(2+)-binding protein (CaBP), induced Ca2+ puffs in resting Xenopus oocytes.

78 fically, there is a calcium binding protein (CaBP)-poor region in the lateral amygdalostriatal area t

79 a separate class of Ca(2+)-binding proteins (CaBP), apparently a major group of CaBP in bacteria.

80 Ca(2+)-binding proteins (CaBPs) are expressed in a highly specific manner across

81 tochemistry for the Ca(2+)-binding proteins (CaBPs) calbindin and calretinin to investigate the prima

82 amily and the related Ca2+-binding proteins (CaBPs) have begun to emerge as key players in neuronal f

83 ons expressing the calcium binding proteins (CaBPs) parvalbumin (PV) and calbindin (CB) have shown ag

84 Calcium-binding proteins (CaBPs) play a buffering role for regulating the concentr

85 and yet the role of Ca(2+) binding proteins (CaBPs) remains elusive.

86 The caldendrins/calcium-binding proteins (CaBPs) represent mammal-specific members of the CaM supe

87 Calcium-binding proteins (CaBPs) such as parvalbumin are part of the cellular calc

88 A family of Ca(2+)-binding proteins (CaBPs) was shown to bind to the inositol 1,4,5-trisphosp

89 stributions of two calcium-binding proteins (CaBPs), calbindinD28k (CB) and parvalbumin (PV), in the

90 e great variety of calcium-binding proteins (CaBPs), many of them contain the same Ca(2+)-binding hel

91 edictably affected by Ca2+-binding proteins (CaBPs).

92 such punctate Co(2+) uptake and of punctate CaBP staining as soon as 4 days postlesion.

93 lacia, accompanied by 90% reduction in renal CaBP-D9k expression but little change in CaBP-D28k.

94 +)-binding proteins in the brain and retina (CaBPs) as essential modulators of voltage-gated Ca(2+) c

95 ength of the rhythm and the number of spared CaBP cells.

96 of a novel Ca(2+)-binding protein subfamily (CaBP), with 46-58% sequence similarity to calmodulin (Ca

97 These results directly demonstrate that CaBP-D28k plays a critical role in maintaining calcium h

98 These results provide evidence that CaBP expression in OT neurons is both greater and more d

99 These data indicate that CaBP plays a direct role in placental calcium transport,

100 However, recent genetic studies suggest that CaBP-D28k is not essential for calcium metabolism.

101 Here, we demonstrate that CaBPs differentially modify Ca(2+) feedback to Ca(v)1.3

102 The CaBP-poor dorsolateral Str region occupies a small porti

103 Approximately 30% of the neurons in both the CaBP-rich border and the caudomedial GP regions project

104 albindin-28K (CaBP) was used to identify the CaBP-poor sensorimotor and CaBP-rich associative Str reg

105 fewer GABAergic neurons were present in the CaBP-dense interclusteral regions of VP and in VPI and P

106 Approximately 40% of neurons in the CaBP-poor middle GP region project to the CaBP-poor part

107 Quantitative analysis of the CaBP distributions reinforced our observations that thes

108 ndicate that pacemakers in the region of the CaBP subnucleus are necessary and sufficient for the con

109 Most of the CaBP-immunoreactive cells in the SGL were small bipolar

110 The complementarity of the CaBP-immunoreactive tiers was also confirmed by fluoresc

111 he CaBP-poor middle GP region project to the CaBP-poor part of the dorsolateral Str.

112 Amygdaloid inputs to the CaBP-poor zone in the lateral amygdalostriatal area aris

113 nd the caudomedial GP regions project to the CaBP-rich Str region.

114 pies a small portion of the Str, whereas the CaBP-poor middle GP region occupies a large portion of t

115 ll Ca++-permeable neurons possess any of the CaBPs examined.

116 hod to investigate the colocalization of the CaBPs, calbindin and calretinin in oxytocin (OT)- and (V

117 he cerebral cortex, neurons expressing these CaBPs express markers of gamma-aminobutyric acidergic ne

118 There are also amygdaloid inputs to CaBP-positive areas outside the shell, which originate m

119 ructural contexts of present day DxDxDG-type CaBPs.

120 is compensated by CaBP-D9k, we generated VDR/CaBP-D28k double knockout (KO) mice, which expressed no

121 d in neurological conditions associated with CaBP deregulation may reflect the loss of necessary stru

122 distribution and morphology of neurons with CaBPs, including calretinin, calbindin, and parvalbumin,