Regulation of the Plasma Membrane Calcium Pump Gene Expression by Two Signal Transduction Pathways

1993 ◽  
Vol 305 (2) ◽  
pp. 428-433 ◽  
Author(s):  
T.H. Kuo ◽  
B.F. Liu ◽  
C. Diglio ◽  
W. Tsang
Keyword(s):  
Gene Expression ◽  
Signal Transduction ◽  
Plasma Membrane ◽  
Calcium Pump ◽  
Signal Transduction Pathways ◽  
Plasma Membrane Calcium Pump

Co-ordinated regulation of the plasma membrane calcium pump and the sarco(endo)plasmic reticular calcium pump gene expression by Ca2+

Cell Calcium ◽  
1997 ◽  
Vol 21 (6) ◽  
pp. 399-408 ◽  
Author(s):  
Tuan H. Kuo ◽  
Bei-Fang Liu ◽  
Yingjie Yu ◽  
Frank Wuytack ◽  
Luc Raeymaekers ◽  
...  
Keyword(s):  
Gene Expression ◽  
Plasma Membrane ◽  
Calcium Pump ◽  
Plasma Membrane Calcium Pump

Positive charge modifications alter the ability of XIP to inhibit the plasma membrane calcium pump

1996 ◽  
Vol 271 (3) ◽  
pp. C736-C741 ◽  
Author(s):  
W. Xu ◽  
C. Gatto ◽  
M. A. Milanick
Keyword(s):  
Plasma Membrane ◽  
Positive Charge ◽  
Calcium Pump ◽  
Inhibitory Peptide ◽  
Ca Pump ◽  
Contact Points ◽  
Plasma Membrane Calcium Pump ◽  
Peptide Analogues ◽  
Positively Charged

Exchange inhibitory peptide (XIP; RRLLFYKYVYKRYRAGKQRG) is the shortest peptide that inhibits the plasma membrane Ca pump at high Ca (A. Enyedi, T. Vorherr, P. James, D. J. McCormick, A. G. Filoteo, E. Carafoli, and J. T. Penniston, J. Biol. Chem. 264: 12313-12321, 1989). Sulfosuccinimidyl acetate (SNA)-modified XIP does not inhibit the Ca pump; SNA neutralizes the positive charge on Lys at positions 7, 11, and 17. Peptide 2CK-XIP (RRLLFYRYVYRCYCAGRQKG) inhibits the pump, but the iodoacetamido-modified peptide does not inhibit. Three peptide analogues, in which 7, 11, and 17 were Ala, Cys, or Lys, inhibited about as well as XIP. SNA modification of these analogues (each with 1 Lys) did not inhibit. SNA modification of 2CK-XIP results in a peptide that does not inhibit; thus position 19 is important. Our results suggest that it is critical that position 19 be positively charged, that positions 7, 11, and 17 are important contact points between XIP and the Ca pump (with at least one positively charged), and that, whereas it is not essential that residues 12 and 14 be positive, they cannot be negative.

scholarly journals Iodide- and Glucose-Handling Gene Expression Regulated by Sorafenib or Cabozantinib in Papillary Thyroid Cancer

2015 ◽  
Vol 100 (5) ◽  
pp. 1771-1779 ◽  
Author(s):  
Maomei Ruan ◽  
Min Liu ◽  
Qianggang Dong ◽  
Libo Chen
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Signal Transduction ◽  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Western Blot ◽  
Glucose Transporter ◽  
Signal Transduction Pathways ◽  
Papillary Thyroid ◽  
Cycle Arrest

Abstract Context: The aberrant silencing of iodide-handling genes accompanied by up-regulation of glucose metabolism presents a major challenge for radioiodine treatment of papillary thyroid cancer (PTC). Objective: This study aimed to evaluate the effect of tyrosine kinase inhibitors on iodide-handling and glucose-handling gene expression in BHP 2-7 cells harboring RET/PTC1 rearrangement. Main Outcome Measures: In this in vitro study, the effects of sorafenib or cabozantinib on cell growth, cycles, and apoptosis were investigated by cell proliferation assay, cell cycle analysis, and Annexin V-FITC apoptosis assay, respectively. The effect of both agents on signal transduction pathways was evaluated using the Western blot. Quantitative real-time PCR, Western blot, immunofluorescence, and radioisotope uptake assays were used to assess iodide-handling and glucose-handling gene expression. Results: Both compounds inhibited cell proliferation in a time-dependent and dose-dependent manner and caused cell cycle arrest in the G0/G1 phase. Sorafenib blocked RET, AKT, and ERK1/2 phosphorylation, whereas cabozantinib blocked RET and AKT phosphorylation. The restoration of iodide-handling gene expression and inhibition of glucose transporter 1 and 3 expression could be induced by either drug. The robust expression of sodium/iodide symporter induced by either agent was confirmed, and 125I uptake was correspondingly enhanced. 18F-fluorodeoxyglucose accumulation was significantly decreased after treatment by either sorafenib or cabozantinib. Conclusions: Sorafenib and cabozantinib had marked effects on cell proliferation, cell cycle arrest, and signal transduction pathways in PTC cells harboring RET/PTC1 rearrangement. Both agents could be potentially used to enhance the expression of iodide-handling genes and inhibit the expression of glucose transporter genes.

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