ライフサイエンスコーパス: TRalpha

1 TRalpha also regulates ApoER2.

2 TRalpha and LXRbeta bind to identical response elements

3 TRalpha export is not sensitive to treatment with the CR

4 TRalpha expression was also increased in human infants w

5 TRalpha was sumoylated at lysines 283 and 389, and TRbet

6 TRalpha-SUMO conjugation utilized the E3 ligase PIASxbet

7 vidence that highlights central roles for 1) TRalpha isoforms in fetal myogenesis, 2) the ratio TRalp

8 in fetal myogenesis, 2) the ratio TRalpha 1:TRalpha 2 in determining cardiac and skeletal muscle phe

9 nificant differences in the ratios TRalpha 1:TRalpha 2, and TRbeta 1:TRbeta 2.

10 mpetition, and (iii) upon loss of PGC-1alpha-TRalpha interactions, PGC-1alpha remains associated with

11 ing, which is mediated by TH receptor alpha (TRalpha) and TRbeta.

12 ative of the thyroid hormone receptor alpha (TRalpha) carried by the avian erythroblastosis virus, co

13 urified with thyroid hormone receptor alpha (TRalpha) from ligand-treated HeLa (alpha-2) cells.

14 ation in the thyroid hormone receptor alpha (TRalpha) gene producing a dominant-negative TRalpha muta

15 LXRbeta) and thyroid hormone receptor alpha (TRalpha), have been found to be essential for correct mi

16 The thyroid hormone receptor alpha1 (TRalpha) exhibits a dual role as an activator or repress

17 k also occurred between transfected PR-B and TRalpha or TRbeta and vice versa in CV1 cells.

18 lpha 1, TRbeta 1, TRbeta 2 (TH binding), and TRalpha 2 (non-TH binding) in functionally distinct porc

19 Here, we have employed the PPARgamma- and TRalpha-activated brown adipose tissue-specific UCP-1 en

20 strate that coexpression of RevErbAalpha and TRalpha regulates the TRalpha1/TRalpha2 ratio in intact

21 tics in response to T3 and is proposed to be TRalpha regulated whereas the other has intermediate ind

22 Both TRalpha and TRbeta bound the full and the half-site ERE

23 eotide sequence variation was found for both TRalpha and TRbeta, with several nonsynonomous substitut

24 By using an antibody that recognizes both TRalpha and TRbeta, we found that TR binding to the TRbe

25 may influence transcriptional regulation by TRalpha isoforms.

26 ole for TRbeta that cannot be substituted by TRalpha in the T3-dependent feedback regulation of TSH t

27 ability to follow the export pathway used by TRalpha has been lost by the oncoprotein during its evol

28 ys to investigate the export pathway used by TRalpha.

29 ted transcription both in transfected cells (TRalpha) and in cell free transcription systems (TRalpha

30 in the same PV mutation to the corresponding TRalpha gene locus to compare the phenotypes of TRalpha1

31 hyroid hormone receptor isotypes, designated TRalpha and TRbeta.

32 st an order of magnitude better than it does TRalpha.

33 In gel mobility shift experiments, TRalpha, retinoid X receptor-alpha, and mature SREBP-1 f

34 ochemistry with confocal microscopy we found TRalpha expressed throughout the tadpole brain, with str

35 (ii) MED1/Mediator displaces PGC-1alpha from TRalpha through LXXLL domain competition, and (iii) upon

36 ear receptors that are encoded by two genes, TRalpha and TRbeta.

37 ear receptors that are encoded by two genes, TRalpha and TRbeta.

38 , in addition to shuttling in heterokaryons, TRalpha shuttles rapidly in an unfused monokaryon system

39 es such as the hindlimbs, which express high TRalpha levels.

40 rvations are consistent with defective human TRalpha-mediated thyroid hormone resistance and substant

41 results, TRAP220 moderately stimulates human TRalpha-mediated transcription in transfected cells, whe

42 duced a greater suppression of serum T(4) in TRalpha(o/o) than it did in WT mice and reduced by a gre

43 We produced mice completely deficient in TRalpha (TRalpha(o/o)) that maintain normal serum thyroi

44 responses to L-T3 were absent or reduced in TRalpha(o/o), whereas they were similar in WT and TRbeta

45 produced significantly greater responses in TRalpha(o/o) and smaller responses in TRbeta(-/-) as com

46 ne, L-T3) given to TH-deprived and to intact TRalpha(o/o) mice.

47 TR isoforms varied markedly between muscles; TRalpha expression was considerably greater than TRbeta

48 (TRalpha) gene producing a dominant-negative TRalpha mutant receptor with a proline to histidine subs

49 of human KCNH2 channels and TRbeta, but not TRalpha, receptors.

50 Ligand-occupied TRalpha or TRbeta, but not the unliganded receptor, stro

51 TRalpha3, another naturally occurring TRalpha isoform whose ninth heptad differs from those of

52 -1 induction, as well as the accumulation of TRalpha, PPARgamma, PGC-1alpha, and MED1 on the UCP-1 en

53 mportant aspect of the shuttling activity of TRalpha is its ability to exit the nucleus through the n

54 taken a comprehensive expression analysis of TRalpha 1, TRbeta 1, TRbeta 2 (TH binding), and TRalpha

55 ved despite the disruption of DNA binding of TRalpha and TRbeta, most notably heart rate, body temper

56 on was markedly reduced in the cerebellum of TRalpha(PV/+) mice but not TRbeta(PV/PV) mice.

57 Deletion of TRalpha 1 reduced them, whereas deletion of TRbeta actua

58 ed intronic sequences as key determinants of TRalpha mRNA processing.

59 t, a portion of the ligand-binding domain of TRalpha and TRbeta was cloned and sequenced for DNA samp

60 In contrast, nuclear export of TRalpha and another isoform, TRbeta, is CRM1-independent

61 both WT and LXRbeta(-/-) mice, expression of TRalpha was high at postnatal day 2.

62 A, which encodes a dominant-negative form of TRalpha, decreases as OPCs proliferate in vitro and in v

63 However, the in vivo functions of TRalpha and TRbeta are undefined.

64 In the first experiment, the inheritance of TRalpha and TRbeta genotypes was determined for metamorp

65 We analyzed involvement of TRalpha and TRbeta in neural cell proliferation during m

66 ide evidence that the inhibitory isoforms of TRalpha are unlikely to play a part in the timing of OPC

67 xis with resistance to TH, while mutation of TRalpha causes a severe delay in skeletal development, t

68 In the presence of TRalpha, a T3 induction ratio of almost 4.0 was found, a

69 A region of TRalpha containing the DNA-binding domain plus flanking

70 eta was ligand-dependent, and sumoylation of TRalpha was ligand-independent.

71 tions are mediated through the C terminus of TRalpha and (at least in part) the LXXLL domains of TRAP

72 e in facilitating efficient translocation of TRalpha from the nucleus to cytoplasm.

73 d with a plasmid containing F2-TRE-TK-CAT or TRalpha, chloramphenicol acetyltransferase expression wa

74 a isoforms in fetal myogenesis, 2) the ratio TRalpha 1:TRalpha 2 in determining cardiac and skeletal

75 e were significant differences in the ratios TRalpha 1:TRalpha 2, and TRbeta 1:TRbeta 2.

76 We found that the thyroid hormone receptor (TRalpha 3) has a differential expression profile.

77 The constitutive thyroid hormone receptor (TRalpha) and its heterodimeric partners (RXRalpha and RX

78 that do not activate the wild-type receptors TRalpha and TRbeta.

79 by two genes encoding the related receptors, TRalpha and TRbeta.

80 ors, i.e. RARalpha, beta and gamma, RXRbeta, TRalpha and TRbeta, to bind various EREs in vitro .

81 eptors (TR) of which there are two subtypes, TRalpha and TRbeta.

82 pha) and in cell free transcription systems (TRalpha and vitamin D receptor).

83 ormones are generally constant, we find that TRalpha and beta dramatically cycle, suggesting that fun

84 and point to the intriguing possibility that TRalpha follows a cooperative export pathway in which bo

85 LXRbeta(-/-) mouse and the possibility that TRalpha may be involved are the subjects of the present

86 Furthermore, our data show that TRalpha directly interacts with calreticulin, and point

87 s, transient transfection assays showed that TRalpha failed to support triiodothyronine (T3)-stimulat

88 Previously, we have shown that TRalpha, formerly thought to reside solely in the nucleu

89 The TRalpha gene encodes T(3)-activated TRalpha1 (NR1A1a) as

90 s a possible link between IGF1/IGF1R and the TRalpha 3 and that over expression of IGF1R in RTT cells

91 ceptor transcription factors, encoded by the TRalpha (NR1A1) and TRbeta (NR1A2) genes, to regulate ta

92 In conclusion, the TRalpha P398H mutation is associated with visceral adipo

93 an diseases associated with mutations in the TRalpha gene and, furthermore, to understand the molecul

94 ever, it is unknown whether mutations in the TRalpha gene could lead to a similar disease.

95 The observed phenotype in the TRalpha P398H mouse is likely due to interference with T

96 viable, indicating that the mutation of the TRalpha gene is not embryonic lethal.

97 Several of the TRalpha HCC mutations also altered the DNA recognition p

98 esent the atomic resolution structure of the TRalpha*T3:RXRalpha*9-cis retinoic acid (9c) ligand bind

99 TRAPs to TRalpha during the function of the TRalpha-TRAP complex and, further, that TRAP220 (possibl

100 one receptor kindred PV (PV) mutation to the TRalpha gene locus by means of homologous recombination

101 show that (i) PGC-1alpha is recruited to the TRalpha-RXRalpha-UCP-1 enhancer complex through interact

102 Lastly, treatment with the TRalpha selective agonist CO23 increased brain cell prol

103 thod in mice with a mutation in either their TRalpha or TRbeta gene.

104 Thus, TRalpha absence with high levels of Dio3 provides double

105 cation of TR by conjugation of small SUMO to TRalpha and TRbeta plays an important role in triiodothy

106 ays a major role in anchoring other TRAPs to TRalpha during the function of the TRalpha-TRAP complex

107 oduced mice completely deficient in TRalpha (TRalpha(o/o)) that maintain normal serum thyroid-stimula

108 ence for the mutant receptors over wild-type TRalpha(wt), that is associated with the cardiotoxic act

109 can be worsened by an increase in unliganded TRalpha.

110 brain predominantly, if not exclusively, via TRalpha.

111 It is unknown whether TRalpha, TRbeta or other receptors are targets for inhib

112 teraction of an N-terminal LXXLL domain with TRalpha, (ii) MED1/Mediator displaces PGC-1alpha from TR

113 s a direct ligand-dependent interaction with TRalpha, and these interactions are mediated through the

114 s 300-389) was required for interaction with TRalpha.

115 98H mouse is likely due to interference with TRalpha action as well as influence on other metabolic s