s2013 Search Results


pf4618433  (Selleck Chemicals)
95
Selleck Chemicals pf4618433
(A) Human islets (n = 3 donors, 10 IEQ/condition) were treated with DHT for 5 min, 30 min, and 18 h, compared with control untreated islets, and studied by RPPA. Normalized values from the three individual donors were averaged to generate an average Z score and map phosphoproteins in the heatmap. *p < 0.05 (t test). (B–H) GSIS was measured in static incubation in male human islets (10 IEQ/condition measured in triplicate) cultured for 24 h with vehicle or DHT (10 nM) followed by 40 min with DHT in the presence or absence of the following inhibitors: (B) dual FAK and PYK2 inhibitors PF431396 (15 nM) and PF562271 (15 nM) (n = 3–5 donors), (C) selective FAK inhibitor PF573228 (10 nM) (n = 3–7 donors), (D) selective PYK2 inhibitor <t>PF4618433</t> (1 μM) (n = 3–7 donors), (E) SRC kinase inhibitor PP2 (1 μM) (n = 3–5 donors), (F) PI3K inhibitors BKM120 (1 μM) and GDC-0941 (1 μM) (n = 3–4 donors), and (H) mTORC2 inhibitor JR-AB2–011 (5 μM) (n = 5 donors). (G) GSIS was measured in static incubation in islets treated with vehicle or DHT (10 nM) for 40 min from male control (RIP-Cre), βRA HET , and βRA KO mice (n = 7 mice, with each condition measured in triplicate, n = 10 islets per replicate),. (I) Representative transmission electron micrographs of human islet β cell treated with vehicle (left) and DHT (right). Insets highlight insulin granules, where red arrows show multigranules. Scale bar, 1 μm. (J) (Top) Quantification of insulin granule size. (Bottom) Quantification of percentage of insulin multigranules over total insulin granules/cell across n = 3 donors (I and J) and 15 cells. (K) Plasma membrane content of VAMP2 normalized for STX4 in INS-1 832/3 cells treated with DHT (10 nM). (L and M) Insulin exocytosis measured by change in capacitance (fF) from human islet β cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Changes in fF are normalized to cell size (pF). (N and O) Calcium current measured in human islet b cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Calcium current (I Ca ), calcium influx (Q Ca ), and calcium influx (pC) are normalized to cell size (pF). (P) Schematic representation of proposed mechanism. (1 and 2) DHT-activated AR pools in the PM vicinity, mitochondria (mito), and nucleus program glycolysis and TCA cycle, increasing CO 2 production, which is converted to HCO 3 − via carbonic anhydrase (CA). HCO 3 − activates the sAC at (3) the PM and (4) endo while CFTR and NBC promote HCO 3 − efflux to maintain pH homeostasis. In parallel, DHT-activated AR pools at the (3) PM and (4) endo collaborate with ligand-activated GLP-1R to promote Gα s recruitment to AR and GLP-1R complexes and activate tmAC. Together, this results in DHT enhancing GLP-1-mediated cAMP production at the PM and endo, which (5) activates cAMP-dependent effectors PKA and EPAC2 to promote insulin granule exocytosis. (6) DHT-activated AR in the PM vicinity activates a signaling cascade including FAK/SRC/PI3K/mTORC2 that further enhances insulin granule exocytosis. AR-DHT may also promote actin remodeling via gelsolin (GSN). Values represent mean ± SE. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
Pf4618433, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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256 hash coprocessor atmel's (2013)  (Atmel Corporation)
90
Atmel Corporation 256 hash coprocessor atmel's (2013)
(A) Human islets (n = 3 donors, 10 IEQ/condition) were treated with DHT for 5 min, 30 min, and 18 h, compared with control untreated islets, and studied by RPPA. Normalized values from the three individual donors were averaged to generate an average Z score and map phosphoproteins in the heatmap. *p < 0.05 (t test). (B–H) GSIS was measured in static incubation in male human islets (10 IEQ/condition measured in triplicate) cultured for 24 h with vehicle or DHT (10 nM) followed by 40 min with DHT in the presence or absence of the following inhibitors: (B) dual FAK and PYK2 inhibitors PF431396 (15 nM) and PF562271 (15 nM) (n = 3–5 donors), (C) selective FAK inhibitor PF573228 (10 nM) (n = 3–7 donors), (D) selective PYK2 inhibitor <t>PF4618433</t> (1 μM) (n = 3–7 donors), (E) SRC kinase inhibitor PP2 (1 μM) (n = 3–5 donors), (F) PI3K inhibitors BKM120 (1 μM) and GDC-0941 (1 μM) (n = 3–4 donors), and (H) mTORC2 inhibitor JR-AB2–011 (5 μM) (n = 5 donors). (G) GSIS was measured in static incubation in islets treated with vehicle or DHT (10 nM) for 40 min from male control (RIP-Cre), βRA HET , and βRA KO mice (n = 7 mice, with each condition measured in triplicate, n = 10 islets per replicate),. (I) Representative transmission electron micrographs of human islet β cell treated with vehicle (left) and DHT (right). Insets highlight insulin granules, where red arrows show multigranules. Scale bar, 1 μm. (J) (Top) Quantification of insulin granule size. (Bottom) Quantification of percentage of insulin multigranules over total insulin granules/cell across n = 3 donors (I and J) and 15 cells. (K) Plasma membrane content of VAMP2 normalized for STX4 in INS-1 832/3 cells treated with DHT (10 nM). (L and M) Insulin exocytosis measured by change in capacitance (fF) from human islet β cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Changes in fF are normalized to cell size (pF). (N and O) Calcium current measured in human islet b cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Calcium current (I Ca ), calcium influx (Q Ca ), and calcium influx (pC) are normalized to cell size (pF). (P) Schematic representation of proposed mechanism. (1 and 2) DHT-activated AR pools in the PM vicinity, mitochondria (mito), and nucleus program glycolysis and TCA cycle, increasing CO 2 production, which is converted to HCO 3 − via carbonic anhydrase (CA). HCO 3 − activates the sAC at (3) the PM and (4) endo while CFTR and NBC promote HCO 3 − efflux to maintain pH homeostasis. In parallel, DHT-activated AR pools at the (3) PM and (4) endo collaborate with ligand-activated GLP-1R to promote Gα s recruitment to AR and GLP-1R complexes and activate tmAC. Together, this results in DHT enhancing GLP-1-mediated cAMP production at the PM and endo, which (5) activates cAMP-dependent effectors PKA and EPAC2 to promote insulin granule exocytosis. (6) DHT-activated AR in the PM vicinity activates a signaling cascade including FAK/SRC/PI3K/mTORC2 that further enhances insulin granule exocytosis. AR-DHT may also promote actin remodeling via gelsolin (GSN). Values represent mean ± SE. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
256 Hash Coprocessor Atmel's (2013), supplied by Atmel Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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petrochina's 2013 annual report  (PetroChina Co Ltd)
90
PetroChina Co Ltd petrochina's 2013 annual report
(A) Human islets (n = 3 donors, 10 IEQ/condition) were treated with DHT for 5 min, 30 min, and 18 h, compared with control untreated islets, and studied by RPPA. Normalized values from the three individual donors were averaged to generate an average Z score and map phosphoproteins in the heatmap. *p < 0.05 (t test). (B–H) GSIS was measured in static incubation in male human islets (10 IEQ/condition measured in triplicate) cultured for 24 h with vehicle or DHT (10 nM) followed by 40 min with DHT in the presence or absence of the following inhibitors: (B) dual FAK and PYK2 inhibitors PF431396 (15 nM) and PF562271 (15 nM) (n = 3–5 donors), (C) selective FAK inhibitor PF573228 (10 nM) (n = 3–7 donors), (D) selective PYK2 inhibitor <t>PF4618433</t> (1 μM) (n = 3–7 donors), (E) SRC kinase inhibitor PP2 (1 μM) (n = 3–5 donors), (F) PI3K inhibitors BKM120 (1 μM) and GDC-0941 (1 μM) (n = 3–4 donors), and (H) mTORC2 inhibitor JR-AB2–011 (5 μM) (n = 5 donors). (G) GSIS was measured in static incubation in islets treated with vehicle or DHT (10 nM) for 40 min from male control (RIP-Cre), βRA HET , and βRA KO mice (n = 7 mice, with each condition measured in triplicate, n = 10 islets per replicate),. (I) Representative transmission electron micrographs of human islet β cell treated with vehicle (left) and DHT (right). Insets highlight insulin granules, where red arrows show multigranules. Scale bar, 1 μm. (J) (Top) Quantification of insulin granule size. (Bottom) Quantification of percentage of insulin multigranules over total insulin granules/cell across n = 3 donors (I and J) and 15 cells. (K) Plasma membrane content of VAMP2 normalized for STX4 in INS-1 832/3 cells treated with DHT (10 nM). (L and M) Insulin exocytosis measured by change in capacitance (fF) from human islet β cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Changes in fF are normalized to cell size (pF). (N and O) Calcium current measured in human islet b cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Calcium current (I Ca ), calcium influx (Q Ca ), and calcium influx (pC) are normalized to cell size (pF). (P) Schematic representation of proposed mechanism. (1 and 2) DHT-activated AR pools in the PM vicinity, mitochondria (mito), and nucleus program glycolysis and TCA cycle, increasing CO 2 production, which is converted to HCO 3 − via carbonic anhydrase (CA). HCO 3 − activates the sAC at (3) the PM and (4) endo while CFTR and NBC promote HCO 3 − efflux to maintain pH homeostasis. In parallel, DHT-activated AR pools at the (3) PM and (4) endo collaborate with ligand-activated GLP-1R to promote Gα s recruitment to AR and GLP-1R complexes and activate tmAC. Together, this results in DHT enhancing GLP-1-mediated cAMP production at the PM and endo, which (5) activates cAMP-dependent effectors PKA and EPAC2 to promote insulin granule exocytosis. (6) DHT-activated AR in the PM vicinity activates a signaling cascade including FAK/SRC/PI3K/mTORC2 that further enhances insulin granule exocytosis. AR-DHT may also promote actin remodeling via gelsolin (GSN). Values represent mean ± SE. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
Petrochina's 2013 Annual Report, supplied by PetroChina Co Ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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kezar's (2013) review of empirical research on sloa  (Kezar Life Sciences)
90
Kezar Life Sciences kezar's (2013) review of empirical research on sloa
(A) Human islets (n = 3 donors, 10 IEQ/condition) were treated with DHT for 5 min, 30 min, and 18 h, compared with control untreated islets, and studied by RPPA. Normalized values from the three individual donors were averaged to generate an average Z score and map phosphoproteins in the heatmap. *p < 0.05 (t test). (B–H) GSIS was measured in static incubation in male human islets (10 IEQ/condition measured in triplicate) cultured for 24 h with vehicle or DHT (10 nM) followed by 40 min with DHT in the presence or absence of the following inhibitors: (B) dual FAK and PYK2 inhibitors PF431396 (15 nM) and PF562271 (15 nM) (n = 3–5 donors), (C) selective FAK inhibitor PF573228 (10 nM) (n = 3–7 donors), (D) selective PYK2 inhibitor <t>PF4618433</t> (1 μM) (n = 3–7 donors), (E) SRC kinase inhibitor PP2 (1 μM) (n = 3–5 donors), (F) PI3K inhibitors BKM120 (1 μM) and GDC-0941 (1 μM) (n = 3–4 donors), and (H) mTORC2 inhibitor JR-AB2–011 (5 μM) (n = 5 donors). (G) GSIS was measured in static incubation in islets treated with vehicle or DHT (10 nM) for 40 min from male control (RIP-Cre), βRA HET , and βRA KO mice (n = 7 mice, with each condition measured in triplicate, n = 10 islets per replicate),. (I) Representative transmission electron micrographs of human islet β cell treated with vehicle (left) and DHT (right). Insets highlight insulin granules, where red arrows show multigranules. Scale bar, 1 μm. (J) (Top) Quantification of insulin granule size. (Bottom) Quantification of percentage of insulin multigranules over total insulin granules/cell across n = 3 donors (I and J) and 15 cells. (K) Plasma membrane content of VAMP2 normalized for STX4 in INS-1 832/3 cells treated with DHT (10 nM). (L and M) Insulin exocytosis measured by change in capacitance (fF) from human islet β cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Changes in fF are normalized to cell size (pF). (N and O) Calcium current measured in human islet b cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Calcium current (I Ca ), calcium influx (Q Ca ), and calcium influx (pC) are normalized to cell size (pF). (P) Schematic representation of proposed mechanism. (1 and 2) DHT-activated AR pools in the PM vicinity, mitochondria (mito), and nucleus program glycolysis and TCA cycle, increasing CO 2 production, which is converted to HCO 3 − via carbonic anhydrase (CA). HCO 3 − activates the sAC at (3) the PM and (4) endo while CFTR and NBC promote HCO 3 − efflux to maintain pH homeostasis. In parallel, DHT-activated AR pools at the (3) PM and (4) endo collaborate with ligand-activated GLP-1R to promote Gα s recruitment to AR and GLP-1R complexes and activate tmAC. Together, this results in DHT enhancing GLP-1-mediated cAMP production at the PM and endo, which (5) activates cAMP-dependent effectors PKA and EPAC2 to promote insulin granule exocytosis. (6) DHT-activated AR in the PM vicinity activates a signaling cascade including FAK/SRC/PI3K/mTORC2 that further enhances insulin granule exocytosis. AR-DHT may also promote actin remodeling via gelsolin (GSN). Values represent mean ± SE. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
Kezar's (2013) Review Of Empirical Research On Sloa, supplied by Kezar Life Sciences, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mcbride, g.b., stott, r., miller, w., bambic, d. and wuertz, s. 2013  (Wuertz GmbH)
90
Wuertz GmbH mcbride, g.b., stott, r., miller, w., bambic, d. and wuertz, s. 2013
(A) Human islets (n = 3 donors, 10 IEQ/condition) were treated with DHT for 5 min, 30 min, and 18 h, compared with control untreated islets, and studied by RPPA. Normalized values from the three individual donors were averaged to generate an average Z score and map phosphoproteins in the heatmap. *p < 0.05 (t test). (B–H) GSIS was measured in static incubation in male human islets (10 IEQ/condition measured in triplicate) cultured for 24 h with vehicle or DHT (10 nM) followed by 40 min with DHT in the presence or absence of the following inhibitors: (B) dual FAK and PYK2 inhibitors PF431396 (15 nM) and PF562271 (15 nM) (n = 3–5 donors), (C) selective FAK inhibitor PF573228 (10 nM) (n = 3–7 donors), (D) selective PYK2 inhibitor <t>PF4618433</t> (1 μM) (n = 3–7 donors), (E) SRC kinase inhibitor PP2 (1 μM) (n = 3–5 donors), (F) PI3K inhibitors BKM120 (1 μM) and GDC-0941 (1 μM) (n = 3–4 donors), and (H) mTORC2 inhibitor JR-AB2–011 (5 μM) (n = 5 donors). (G) GSIS was measured in static incubation in islets treated with vehicle or DHT (10 nM) for 40 min from male control (RIP-Cre), βRA HET , and βRA KO mice (n = 7 mice, with each condition measured in triplicate, n = 10 islets per replicate),. (I) Representative transmission electron micrographs of human islet β cell treated with vehicle (left) and DHT (right). Insets highlight insulin granules, where red arrows show multigranules. Scale bar, 1 μm. (J) (Top) Quantification of insulin granule size. (Bottom) Quantification of percentage of insulin multigranules over total insulin granules/cell across n = 3 donors (I and J) and 15 cells. (K) Plasma membrane content of VAMP2 normalized for STX4 in INS-1 832/3 cells treated with DHT (10 nM). (L and M) Insulin exocytosis measured by change in capacitance (fF) from human islet β cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Changes in fF are normalized to cell size (pF). (N and O) Calcium current measured in human islet b cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Calcium current (I Ca ), calcium influx (Q Ca ), and calcium influx (pC) are normalized to cell size (pF). (P) Schematic representation of proposed mechanism. (1 and 2) DHT-activated AR pools in the PM vicinity, mitochondria (mito), and nucleus program glycolysis and TCA cycle, increasing CO 2 production, which is converted to HCO 3 − via carbonic anhydrase (CA). HCO 3 − activates the sAC at (3) the PM and (4) endo while CFTR and NBC promote HCO 3 − efflux to maintain pH homeostasis. In parallel, DHT-activated AR pools at the (3) PM and (4) endo collaborate with ligand-activated GLP-1R to promote Gα s recruitment to AR and GLP-1R complexes and activate tmAC. Together, this results in DHT enhancing GLP-1-mediated cAMP production at the PM and endo, which (5) activates cAMP-dependent effectors PKA and EPAC2 to promote insulin granule exocytosis. (6) DHT-activated AR in the PM vicinity activates a signaling cascade including FAK/SRC/PI3K/mTORC2 that further enhances insulin granule exocytosis. AR-DHT may also promote actin remodeling via gelsolin (GSN). Values represent mean ± SE. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
Mcbride, G.B., Stott, R., Miller, W., Bambic, D. And Wuertz, S. 2013, supplied by Wuertz GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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kluemper, d. h., degroot, t., & choi, s. (2013)  (Verlag GmbH)
90
Verlag GmbH kluemper, d. h., degroot, t., & choi, s. (2013)
(A) Human islets (n = 3 donors, 10 IEQ/condition) were treated with DHT for 5 min, 30 min, and 18 h, compared with control untreated islets, and studied by RPPA. Normalized values from the three individual donors were averaged to generate an average Z score and map phosphoproteins in the heatmap. *p < 0.05 (t test). (B–H) GSIS was measured in static incubation in male human islets (10 IEQ/condition measured in triplicate) cultured for 24 h with vehicle or DHT (10 nM) followed by 40 min with DHT in the presence or absence of the following inhibitors: (B) dual FAK and PYK2 inhibitors PF431396 (15 nM) and PF562271 (15 nM) (n = 3–5 donors), (C) selective FAK inhibitor PF573228 (10 nM) (n = 3–7 donors), (D) selective PYK2 inhibitor <t>PF4618433</t> (1 μM) (n = 3–7 donors), (E) SRC kinase inhibitor PP2 (1 μM) (n = 3–5 donors), (F) PI3K inhibitors BKM120 (1 μM) and GDC-0941 (1 μM) (n = 3–4 donors), and (H) mTORC2 inhibitor JR-AB2–011 (5 μM) (n = 5 donors). (G) GSIS was measured in static incubation in islets treated with vehicle or DHT (10 nM) for 40 min from male control (RIP-Cre), βRA HET , and βRA KO mice (n = 7 mice, with each condition measured in triplicate, n = 10 islets per replicate),. (I) Representative transmission electron micrographs of human islet β cell treated with vehicle (left) and DHT (right). Insets highlight insulin granules, where red arrows show multigranules. Scale bar, 1 μm. (J) (Top) Quantification of insulin granule size. (Bottom) Quantification of percentage of insulin multigranules over total insulin granules/cell across n = 3 donors (I and J) and 15 cells. (K) Plasma membrane content of VAMP2 normalized for STX4 in INS-1 832/3 cells treated with DHT (10 nM). (L and M) Insulin exocytosis measured by change in capacitance (fF) from human islet β cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Changes in fF are normalized to cell size (pF). (N and O) Calcium current measured in human islet b cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Calcium current (I Ca ), calcium influx (Q Ca ), and calcium influx (pC) are normalized to cell size (pF). (P) Schematic representation of proposed mechanism. (1 and 2) DHT-activated AR pools in the PM vicinity, mitochondria (mito), and nucleus program glycolysis and TCA cycle, increasing CO 2 production, which is converted to HCO 3 − via carbonic anhydrase (CA). HCO 3 − activates the sAC at (3) the PM and (4) endo while CFTR and NBC promote HCO 3 − efflux to maintain pH homeostasis. In parallel, DHT-activated AR pools at the (3) PM and (4) endo collaborate with ligand-activated GLP-1R to promote Gα s recruitment to AR and GLP-1R complexes and activate tmAC. Together, this results in DHT enhancing GLP-1-mediated cAMP production at the PM and endo, which (5) activates cAMP-dependent effectors PKA and EPAC2 to promote insulin granule exocytosis. (6) DHT-activated AR in the PM vicinity activates a signaling cascade including FAK/SRC/PI3K/mTORC2 that further enhances insulin granule exocytosis. AR-DHT may also promote actin remodeling via gelsolin (GSN). Values represent mean ± SE. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
Kluemper, D. H., Degroot, T., & Choi, S. (2013), supplied by Verlag GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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s 2013 (project 2)  (Amano Inc)
90
Amano Inc s 2013 (project 2)
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S 2013 (Project 2), supplied by Amano Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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shambaugh's (2013) china goes global  (Sino American Shanghai Squibb Pharmaceuticals Co)
90
Sino American Shanghai Squibb Pharmaceuticals Co shambaugh's (2013) china goes global
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Shambaugh's (2013) China Goes Global, supplied by Sino American Shanghai Squibb Pharmaceuticals Co, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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edge-mounted qds in sony's 2013 line of triluminos televisions  (Sony)
90
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narayanan k, makino s. 2013  (Makino Inc)
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Makino Inc narayanan k, makino s. 2013
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Narayanan K, Makino S. 2013, supplied by Makino Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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deloitte's 2013 global supply chain risk survey  (Deloitte LLP)
90
Deloitte LLP deloitte's 2013 global supply chain risk survey
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Deloitte's 2013 Global Supply Chain Risk Survey, supplied by Deloitte LLP, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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schill s. 2013  (Schill Seilacher GmbH)
90
Schill Seilacher GmbH schill s. 2013
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Schill S. 2013, supplied by Schill Seilacher GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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(A) Human islets (n = 3 donors, 10 IEQ/condition) were treated with DHT for 5 min, 30 min, and 18 h, compared with control untreated islets, and studied by RPPA. Normalized values from the three individual donors were averaged to generate an average Z score and map phosphoproteins in the heatmap. *p < 0.05 (t test). (B–H) GSIS was measured in static incubation in male human islets (10 IEQ/condition measured in triplicate) cultured for 24 h with vehicle or DHT (10 nM) followed by 40 min with DHT in the presence or absence of the following inhibitors: (B) dual FAK and PYK2 inhibitors PF431396 (15 nM) and PF562271 (15 nM) (n = 3–5 donors), (C) selective FAK inhibitor PF573228 (10 nM) (n = 3–7 donors), (D) selective PYK2 inhibitor PF4618433 (1 μM) (n = 3–7 donors), (E) SRC kinase inhibitor PP2 (1 μM) (n = 3–5 donors), (F) PI3K inhibitors BKM120 (1 μM) and GDC-0941 (1 μM) (n = 3–4 donors), and (H) mTORC2 inhibitor JR-AB2–011 (5 μM) (n = 5 donors). (G) GSIS was measured in static incubation in islets treated with vehicle or DHT (10 nM) for 40 min from male control (RIP-Cre), βRA HET , and βRA KO mice (n = 7 mice, with each condition measured in triplicate, n = 10 islets per replicate),. (I) Representative transmission electron micrographs of human islet β cell treated with vehicle (left) and DHT (right). Insets highlight insulin granules, where red arrows show multigranules. Scale bar, 1 μm. (J) (Top) Quantification of insulin granule size. (Bottom) Quantification of percentage of insulin multigranules over total insulin granules/cell across n = 3 donors (I and J) and 15 cells. (K) Plasma membrane content of VAMP2 normalized for STX4 in INS-1 832/3 cells treated with DHT (10 nM). (L and M) Insulin exocytosis measured by change in capacitance (fF) from human islet β cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Changes in fF are normalized to cell size (pF). (N and O) Calcium current measured in human islet b cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Calcium current (I Ca ), calcium influx (Q Ca ), and calcium influx (pC) are normalized to cell size (pF). (P) Schematic representation of proposed mechanism. (1 and 2) DHT-activated AR pools in the PM vicinity, mitochondria (mito), and nucleus program glycolysis and TCA cycle, increasing CO 2 production, which is converted to HCO 3 − via carbonic anhydrase (CA). HCO 3 − activates the sAC at (3) the PM and (4) endo while CFTR and NBC promote HCO 3 − efflux to maintain pH homeostasis. In parallel, DHT-activated AR pools at the (3) PM and (4) endo collaborate with ligand-activated GLP-1R to promote Gα s recruitment to AR and GLP-1R complexes and activate tmAC. Together, this results in DHT enhancing GLP-1-mediated cAMP production at the PM and endo, which (5) activates cAMP-dependent effectors PKA and EPAC2 to promote insulin granule exocytosis. (6) DHT-activated AR in the PM vicinity activates a signaling cascade including FAK/SRC/PI3K/mTORC2 that further enhances insulin granule exocytosis. AR-DHT may also promote actin remodeling via gelsolin (GSN). Values represent mean ± SE. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Journal: Cell reports

Article Title: Architecture of androgen receptor pathways amplifying glucagon-like peptide-1 insulinotropic action in male pancreatic β cells

doi: 10.1016/j.celrep.2023.112529

Figure Lengend Snippet: (A) Human islets (n = 3 donors, 10 IEQ/condition) were treated with DHT for 5 min, 30 min, and 18 h, compared with control untreated islets, and studied by RPPA. Normalized values from the three individual donors were averaged to generate an average Z score and map phosphoproteins in the heatmap. *p < 0.05 (t test). (B–H) GSIS was measured in static incubation in male human islets (10 IEQ/condition measured in triplicate) cultured for 24 h with vehicle or DHT (10 nM) followed by 40 min with DHT in the presence or absence of the following inhibitors: (B) dual FAK and PYK2 inhibitors PF431396 (15 nM) and PF562271 (15 nM) (n = 3–5 donors), (C) selective FAK inhibitor PF573228 (10 nM) (n = 3–7 donors), (D) selective PYK2 inhibitor PF4618433 (1 μM) (n = 3–7 donors), (E) SRC kinase inhibitor PP2 (1 μM) (n = 3–5 donors), (F) PI3K inhibitors BKM120 (1 μM) and GDC-0941 (1 μM) (n = 3–4 donors), and (H) mTORC2 inhibitor JR-AB2–011 (5 μM) (n = 5 donors). (G) GSIS was measured in static incubation in islets treated with vehicle or DHT (10 nM) for 40 min from male control (RIP-Cre), βRA HET , and βRA KO mice (n = 7 mice, with each condition measured in triplicate, n = 10 islets per replicate),. (I) Representative transmission electron micrographs of human islet β cell treated with vehicle (left) and DHT (right). Insets highlight insulin granules, where red arrows show multigranules. Scale bar, 1 μm. (J) (Top) Quantification of insulin granule size. (Bottom) Quantification of percentage of insulin multigranules over total insulin granules/cell across n = 3 donors (I and J) and 15 cells. (K) Plasma membrane content of VAMP2 normalized for STX4 in INS-1 832/3 cells treated with DHT (10 nM). (L and M) Insulin exocytosis measured by change in capacitance (fF) from human islet β cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Changes in fF are normalized to cell size (pF). (N and O) Calcium current measured in human islet b cells with DHT (10 nM) applied via patch pipette in the presence of cAMP (100 μM) (n = 22 cells per treatment). Calcium current (I Ca ), calcium influx (Q Ca ), and calcium influx (pC) are normalized to cell size (pF). (P) Schematic representation of proposed mechanism. (1 and 2) DHT-activated AR pools in the PM vicinity, mitochondria (mito), and nucleus program glycolysis and TCA cycle, increasing CO 2 production, which is converted to HCO 3 − via carbonic anhydrase (CA). HCO 3 − activates the sAC at (3) the PM and (4) endo while CFTR and NBC promote HCO 3 − efflux to maintain pH homeostasis. In parallel, DHT-activated AR pools at the (3) PM and (4) endo collaborate with ligand-activated GLP-1R to promote Gα s recruitment to AR and GLP-1R complexes and activate tmAC. Together, this results in DHT enhancing GLP-1-mediated cAMP production at the PM and endo, which (5) activates cAMP-dependent effectors PKA and EPAC2 to promote insulin granule exocytosis. (6) DHT-activated AR in the PM vicinity activates a signaling cascade including FAK/SRC/PI3K/mTORC2 that further enhances insulin granule exocytosis. AR-DHT may also promote actin remodeling via gelsolin (GSN). Values represent mean ± SE. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: Islets were then treated with vehicle (95% ethanol), DHT, GLP-1 (10nM; Indiana University Bloomington), GIP (100nM; Tocris), glucagon (20nM; Sigma), forskolin (10μM; Sigma), H89 (10μM; CST), ESI-09 (10μM; Sigma), Exendin9–39 (100nM; Sigma), KH7 (1μM; Sigma Aldrich), LRE1 (10μM; Sigma Aldrich), TDI-10229 (2μM, 5μM, 10μM; Cornell), Acetazolamide/AZZ (50μM; MedChemExpress), CFTRinh-172 (500μM; Selleckchem), S0859 (2μM; MedChemExpress), 2′,5′-Dideoxyadenosine/ddADO (1μM), PF431396 (15nM; Selleckchem), PF562271 (15nM; Selleckchem) PF573228 (10nM; MedChemExpress), PF4618433 (1μM; MedChemExpress), PP2 (1μM; Sigma Aldrich), BKM120 (1μM; Selleckchem), GDC-0941 (1μM; Sigma Aldrich), Rapamycin (27.4nM; Sigma Aldrich), JR-AB2–011 (5μM; TargetMol), Linagliptin (83 μg/ kg; Boehringer Ingelheim), Finasteride (100nM; Sigma Aldrich), Dutasteride (100nM; Sigma Aldrich), Exendin4 (100nM), ExendinPhe1 (100nM; Imperial College London) at 2.8mM and then 16.7mM glucose for 40 min sequentially.

Techniques: Control, Incubation, Cell Culture, Transmission Assay, Clinical Proteomics, Membrane, Transferring

KEY RESOURCES TABLE

Journal: Cell reports

Article Title: Architecture of androgen receptor pathways amplifying glucagon-like peptide-1 insulinotropic action in male pancreatic β cells

doi: 10.1016/j.celrep.2023.112529

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Islets were then treated with vehicle (95% ethanol), DHT, GLP-1 (10nM; Indiana University Bloomington), GIP (100nM; Tocris), glucagon (20nM; Sigma), forskolin (10μM; Sigma), H89 (10μM; CST), ESI-09 (10μM; Sigma), Exendin9–39 (100nM; Sigma), KH7 (1μM; Sigma Aldrich), LRE1 (10μM; Sigma Aldrich), TDI-10229 (2μM, 5μM, 10μM; Cornell), Acetazolamide/AZZ (50μM; MedChemExpress), CFTRinh-172 (500μM; Selleckchem), S0859 (2μM; MedChemExpress), 2′,5′-Dideoxyadenosine/ddADO (1μM), PF431396 (15nM; Selleckchem), PF562271 (15nM; Selleckchem) PF573228 (10nM; MedChemExpress), PF4618433 (1μM; MedChemExpress), PP2 (1μM; Sigma Aldrich), BKM120 (1μM; Selleckchem), GDC-0941 (1μM; Sigma Aldrich), Rapamycin (27.4nM; Sigma Aldrich), JR-AB2–011 (5μM; TargetMol), Linagliptin (83 μg/ kg; Boehringer Ingelheim), Finasteride (100nM; Sigma Aldrich), Dutasteride (100nM; Sigma Aldrich), Exendin4 (100nM), ExendinPhe1 (100nM; Imperial College London) at 2.8mM and then 16.7mM glucose for 40 min sequentially.

Techniques: Recombinant, Enzyme-linked Immunosorbent Assay, Single Cell, RNA sequencing, Gene Expression, Software, Single-cell Analysis

Characteristics of the participants in the included studies.

Journal: PLoS ONE

Article Title: Efficacy and Safety of Tai Chi for Parkinson's Disease: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

doi: 10.1371/journal.pone.0099377

Figure Lengend Snippet: Characteristics of the participants in the included studies.

Article Snippet: Amano S 2013 (project 2) , Florida, USA , 1 , 24 , 14/10 , 66±11/66±7 , 2.4±0.6/2.4±0.4 , 8±5/5±3.

Techniques:

Characteristics of the included studies.

Journal: PLoS ONE

Article Title: Efficacy and Safety of Tai Chi for Parkinson's Disease: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

doi: 10.1371/journal.pone.0099377

Figure Lengend Snippet: Characteristics of the included studies.

Article Snippet: Amano S 2013 (project 2) , Florida, USA , 1 , 24 , 14/10 , 66±11/66±7 , 2.4±0.6/2.4±0.4 , 8±5/5±3.

Techniques: