thyroid hormone receptor alpha thra  (Proteintech)

Journal: Molecular and cellular endocrinology

Article Title: Exogenous Thyroxine Increases Cardiac GLUT4 Translocation in Insulin Resistant OLETF Rats.

doi: 10.1016/j.mce.2024.112254

Figure Lengend Snippet: Figure 4. Thyroid hormone profile in heart, T4 increased THRB1 in cytosol. Mean ± SD values for (A) Monocarboxylate transporter 8 (MCT8) protein expression, (B) deiodinase 2 (DIO2) protein expression, (C) thyroid hormone receptor beta 1 (THRB1) protein expression, (D) nuclear thyroid hormone receptor alpha (THRa) protein expression and (E) representative blot of LETO, LETO + T4, OLETF, and OLETF + T4 rats (n=6-7) PS, ponceau stain. *, Significant difference from LETO p<0.05. &, Significant difference from OLETF p<0.05. $, Significant difference from LETO + T4 p<0.05. #, Significant difference from OLETF + T4 p<0.05.

Article Snippet: 126 Membranes were incubated with primary antibodies against GLUT4 (Abcam, ab33780, Boston, 127 MA, USA), pS488-GLUT4 (Abcam, ab188317, Boston, MA, USA), insulin receptor (IR) (Cell 128 Signaling Technology, 3025S, USA), insulin receptor substrate (IRS) 1 + IRS 2 (abcam, ab40777, 129 Boston, MA, USA), phosphoinositide 3-kinases p110 (PI3K)p110 (Proteintech, 67071-1-Ig, 130 Rosemont, IL, USA), protein kinase B (AKT) (Cell Signaling Technology, 9272S, USA), p-AKT (Cell 131 Jo urn al Pr e-p roo f REVISED Manuscript (text UNmarked) 7 Signaling Technology, 4060S, USA), anti-AMPK alpha 1 (phospho T183) + AMPK alpha 2 (phospho 132 T172) (Abcam, ab133448, Boston, MA, USA), AKT substrate 160 (AS160) (C69A7) (Cell Signaling 133 Technology, 2670S, USA), Phospho-AS160 (Thr642) (D27E6) (Cell Signaling Technology, 8881S, 134 USA), hexokinase 2 (Proteintech, 22029-1-AP, Rosemont, IL, USA), phosphofructokinase muscle 135 type (PFKM) (Abcam, ab154804, Boston, MA, USA), monocarboxylate transporter 8 (MCT8) 136 (Abcam, ab302706, Boston, MA, USA), Type II iodothyronine deiodinase (DIO2) (Proteintech, 137 26513-1-AP, Rosemont, IL, USA), thyroid hormone receptor β (TRβ1) (Abcam, ab180612, Boston, 138 MA, USA), thyroid hormone receptor alpha (THRa) (Proteintech, 66703-1-Ig, Rosemont, IL, USA), 139 the fatty acid transporter, cluster of differentiation 36 (CD36) (Thermo Fisher, PA1-16813, 140 Houston, TX, USA), fatty acid transporter (FATP1) (MyBioSource, MBS9384813, San Diego, CA, 141 USA), carnitine palmitoyltransferase 2 (CPT2) (Invitrogen, PA5-30420, Waltham, MA, USA), acyl-142 coA oxidase 1 (ACOX) (Thermo Fisher, PA5-76341, USA), acetyl-coA carboxylase 1 (ACC) (Cell 143 Signaling Technology, 3662S, USA), diacylglycerol O-acyltransferase 1 (DGAT1) (Thermo Fisher, 144 PA5-79150, Houston, TX, USA), and glycerol-3-phosphate acyltransferase (GPAM) (abcam, 145 ab69990, Boston, MA, USA).

Techniques: Expressing, Staining

Journal: PLoS ONE

Article Title: Thyroid Hormone Response Element Half-Site Organization and Its Effect on Thyroid Hormone Mediated Transcription

doi: 10.1371/journal.pone.0101155

Figure Lengend Snippet: COS-7 cells were co-transfected with a TRα or TRα+RXRα expression vectors. Cells were treated with or without 5 nM T3, or with T3 in the presence of 10 µM 1–850. Firefly luciferase expression was normalized to renilla luciferase expression. Experiments were run in triplicate and repeated at least 3 times. Data are presented as means ± standard error of the mean. Asterisks (*) denote a significant difference, p≤0.05, determined by one way ANOVA followed by Tukey's HSD test; (ns) denote no significant difference, p≥0.05.

Article Snippet: Twenty-four hours after seeding, cells were transfected using FUGENE HD (Promega) with 100 ng of the reporter plasmid of interest (see ), and co-transfected with 10 ng pRL-CMV(Promega) and 50 ng TRα (SC307938, Origene, MD, USA) with and without 50 ng RXRα (MC216284, Origene).

Techniques: Transfection, Expressing, Luciferase