ライフサイエンスコーパス: c-Fos protein

1 fter mFSS exposure for CRF and AVP mRNAs and c-Fos protein.

2 dissociates c-Fos from KDM2B and stabilizes c-Fos protein.

3 neocortex (GNC) expresses enhanced levels of c-Fos protein.

4 reased levels of c-fos promoter activity and c-fos protein.

5 me associated with massive CNS expression of c-Fos protein.

6 then processed immunohistochemically for the c-Fos protein.

7 neurons were identified through detection of c-Fos protein.

8 ound as a heterodimer comprised of c-Jun and c-Fos proteins.

9 ation and nuclear translocation of EGR-2 and c-fos proteins.

10 ent in JNK activity, had increased c-jun and c-fos proteins.

11 GHF-1 interacted directly with c-Jun but not c-Fos proteins.

12 As expected, Ex4 induced expression of c-Fos protein, a marker of neuronal activation, in hindb

13 .8% standardized green tea extract inhibited c-fos protein accumulation by 18.5% and 46.2% (p < 0.05)

14 behavioral tests and circuit analyses using c-fos protein activation were conducted on the vulnerabl

15 trations in fetal peripheral plasma and Fos (c-fos protein) activation in corticotropin-releasing hor

16 nslational modification of newly synthesized c-Fos protein after H2O2 exposure.

17 activity and accumulation of c-fos mRNA and c-Fos protein after UVB irradiation.

18 stibular neurons were conducted to visualize c-Fos protein and Fluoro-Gold concomitantly.

19 in (i.e. PP2B), resulted in disappearance of c-Fos protein and MG132 was able to prevent this loss.

20 lpha-dihydrotestosterone and R1881) suppress c-Fos protein and mRNA expression induced by 12-O-tetrad

21 ity involving transient de novo synthesis of c-Fos protein and prolonged synthesis of c-Jun, mediated

22 tochemistry for NMDA NR1 glutamate receptor, c-fos protein, and apoptosis [nuclear immunoreactivity f

23 In addition, we used the expression of c-Fos protein as a marker of neuronal activity to assess

24 The present study used the expression of c-Fos protein as a marker to identify brain areas throug

25 re, expression of either wild-type or mutant c-fos proteins augmented or diminished the response of t

26 increased the expression of the AP-1 subunit c-Fos protein, but not in the presence of PD98095 and wo

27 by in situ hybridization) and immunoreactive c-Fos protein (by immunohistochemistry) were elevated by

28 cells in serum-free medium, indicating that c-Fos protein can induce apoptotic cell death in these c

29 quence similarity with AREs, the purine-rich c-fos protein-coding region determinant of instability.

30 pid increase in c-fos mRNA, but the level of c-Fos protein decreases due to degradation by the multic

31 tion by assembling an E3 ligase to targeting c-Fos protein degradation that is antagonized by mitogen

32 hosphorylation contributes to degradation of c-Fos protein during oxidative stress response of cardio

33 er cypermethrin, extended the time course of c-Fos protein elevation after H2O2 exposure.

34 some Inhibitor I extended the time course of c-Fos protein elevation.

35 e perfused either 5 min or 2 h after SCS and c-fos protein examined immunohistochemically.

36 Here we report that cortical c-Fos protein expression declines significantly followin

37 Histological examination of c-Fos protein expression identified brain regions that r

38 ata show a dynamic and nonuniform pattern of c-Fos protein expression in brain nuclei known to mediat

39 We used the activation of c-fos protein expression in spinally projecting neurons

40 , MK801, partially reduces cocaine-activated c-Fos protein expression in the CPu.

41 iated with lithium chloride-induced malaise, c-Fos protein expression increased dramatically as compa

42 Fos to the p28 promoter but had no effect on c-Fos protein expression or phosphorylation in response

43 nalysis which showed METH-induced changes in c-Fos protein expression that were blocked by pretreatme

44 MMP-9 through increased AP-1/DNA binding and c-Fos protein expression via ERK and PI3K signaling path

45 Using immunohistochemical methods, brain c-Fos protein expression was analyzed in rats that extin

46 on-associated protein (Arc) mRNA and Arc and c-Fos protein expression was detected in RSP from fear-c

47 Immunohistochemical quantification of c-Fos protein expression was used as the surrogate measu

48 5) and were subsequently tested for baseline c-Fos protein expression within the hippocampal subfield

49 ess-induced 5-HT neural activity, indexed by c-Fos protein expression, in the DRN and c-Fos expressio

50 NAc, SCH23390 also inhibits cocaine-induced c-Fos protein expression.

51 -1 DNA binding activity through induction of c-Fos protein expression.

52 DHEA increased c-Jun, but not c-Fos, protein expression after 2 h.

53 ic area (vlPOA) express immunoreactivity for c-Fos protein following sustained sleep, and display ele

54 The c-Fos proteins form heterodimers with Jun family protein

55 failure (HF) by mapping neuronal staining of c-Fos protein (Fos) 6-8 weeks following coronary artery

56 sponsive to novel tastes, immunostaining for c-fos protein (Fos-like immunoreactivity [FLI]) was used

57 The c-fos protein, Fos, was identified immunocytochemically

58 An increase in ubiquitin was detectable in c-Fos protein from H2O2-treated cells.

59 The presence of the c-Fos protein has been evidenced in the piriform cortex,

60 Expression of c-Fos protein immunoreactivity (IR) in GABAergic neurons

61 We examined the pattern of c-Fos protein immunoreactivity throughout the rostral-ca

62 increase in neural activity (as measured by c-fos protein immunoreactivity) when spontaneous recover

63 These results suggest that the decrease in c-Fos protein in cortical neurons during sleep may be at

64 euronal loss, an expression of dynorphin and c-Fos protein in neurons in the deep laminae of the dors

65 fiber primary afferent input, and upregulate c-Fos protein in response to noxious stimuli.

66 s, we examined the patterns of expression of c-Fos protein in the brain and correlated these with phy

67 This study examined the expression of the c-Fos protein in the rabbit's central nervous system to

68 (as indicated by the regional expression of c-Fos protein) in rats during acquisition and throughout

69 Western blot analysis showed that the c-fos protein level increased in the nuclear fraction af

70 c-Fos protein levels are slightly increased in these can

71 kinase, pp90 ribosomal S6 kinase (RSK), and c-Fos protein levels in the caudate/putamen of Fischer r

72 ase in brain-derived neurotrophic factor and c-FOS protein levels, key regulators of synaptic plastic

73 fficient to induce AP-1 and increase nuclear c-Fos protein levels, PI 3-kinase may need to cooperate

74 s c-Fos for polyubiquitylation and regulates c-Fos protein levels.

75 -Fos mRNA but caused no alternation in total c-Fos protein levels.

76 activity and phosphorylation, and increased c-fos protein levels.

77 upershift experiments revealed that JunD and c-Fos proteins mediated anti-CD19 induced AP-1-binding a

78 The TP functionality anchors the c-Fos protein onto the metal substrate and works as an e

79 Chimeric ZEBRA/c-Fos proteins overexpressed in Escherichia coli bound D

80 The data suggest that c-Fos protein plays a causal role in the activation of a

81 ctions, immunohistochemical detection of the c-Fos protein product was used to study the distribution

82 Western blot analyses of c-MYC and c-FOS protein products support the overexpression of the

83 Decreased levels of c-fos protein result in decreased AP-1 activity, as dete

84 c-Fos protein(s) expression was high at 1.5 h and decrea

85 Finally, c-fos protein staining after novelty suppressed feeding

86 t TGFbeta, presumably through its effects on c-Fos protein synthesis and/or stability, abrogates the

87 ted UVB induced c-fos gene transcription and c-Fos protein synthesis.

88 ium release induces a sustained elevation of c-Fos protein that precedes grp78 induction.

89 by increased nuclear abundance of c-jun and c-fos proteins that bound specifically to the proximal c

90 histochemical analysis of rapidly developing c-Fos protein to elucidate neurobiological loci involved

91 the present study we used the expression of c-Fos protein to identify CNS regions activated during i

92 manner, and increased binding of endogenous c-fos protein to the cyclin A CRE precedes the onset of

93 In addition, the amount of c-Fos protein was estimated by chemiluminescent immunobl

94 In reticular formation c-fos protein was induced in circumscribed columns in th

95 Expression of c-Fos protein was not detected in calretinin-positive ne

96 d phosphomimetic mutations at S374 result in c-Fos protein which cannot be induced by EGF or accumula

97 e phosphatase A (PP2A) and immunoblotting of c-Fos protein with antibodies against phosphorylated ser

98 ones are GABAergic by combining staining for c-Fos protein with staining for glutamic acid decarboxyl

99 Treatment of immunoprecipitated c-Fos protein with the type 2 serine/threonine phosphata

100 thesis, including increase of Arc, Egr1, and c-Fos proteins, without affecting their mRNA induction.