Docking is not a prerequisite but a temporal constraint for fusion of secretory granules. - Wikidata - thesis-toulmin - TriplyDB

Docking is not a prerequisite but a temporal constraint for fusion of secretory granules.

Docking is not a prerequisite but a temporal constraint for fusion of secretory granules.

http://www.wikidata.org/entity/Q46657374

about

Distinct initial SNARE configurations underlying the diversity of exocytosis A novel role for the centrosomal protein, pericentrin, in regulation of insulin secretory vesicle docking in mouse pancreatic beta-cells Granuphilin exclusively mediates functional granule docking to the plasma membrane.Preferential release of newly synthesized insulin assessed by a multi-label reporter system using pancreatic β-cell line MIN6 Neurexin-1α contributes to insulin-containing secretory granule docking Exophilin8 transiently clusters insulin granules at the actin-rich cell cortex prior to exocytosis.The Rab27a effector exophilin7 promotes fusion of secretory granules that have not been docked to the plasma membrane.Munc18b is a major mediator of insulin exocytosis in rat pancreatic β-cells Aged insulin granules display reduced microtubule-dependent mobility and are disposed within actin-positive multigranular bodies Systematic Synergy of Glucose and GLP-1 to Stimulate Insulin Secretion Revealed by Quantitative Phosphoproteomics.Small G proteins in islet beta-cell function.Cell signalling in insulin secretion: the molecular targets of ATP, cAMP and sulfonylurea.Altered pancreatic islet function and morphology in mice lacking the Beta-cell surface protein neuroligin-2.Dynamics of insulin secretion and the clinical implications for obesity and diabetes Contact-induced clustering of syntaxin and munc18 docks secretory granules at the exocytosis site.Calcium current inactivation rather than pool depletion explains reduced exocytotic rate with prolonged stimulation in insulin-secreting INS-1 832/13 cells.Coupling of metabolic, second messenger pathways and insulin granule dynamics in pancreatic beta-cells: a computational analysis Vesicle Motion during Sustained Exocytosis in Chromaffin Cells: Numerical Model Based on Amperometric Measurements.COPII-Dependent ER Export: A Critical Component of Insulin Biogenesis and β-Cell ER Homeostasis.Evolving insights regarding mechanisms for the inhibition of insulin release by norepinephrine and heterotrimeric G proteins.Rab27 and Rab3 sequentially regulate human sperm dense-core granule exocytosis Extracellular CADM1 interactions influence insulin secretion by rat and human islet β-cells and promote clustering of syntaxin-1.Newcomer insulin secretory granules as a highly calcium-sensitive pool Rab27a and MyRIP regulate the amount and multimeric state of VWF released from endothelial cells.Synaptotagmins bind calcium to release insulin.Mechanisms of biphasic insulin-granule exocytosis - roles of the cytoskeleton, small GTPases and SNARE proteins.Synaptotagmin-7 Functions to Replenish Insulin Granules for Exocytosis in Human Islet β-Cells.Pancreatic beta-cell signaling: toward better understanding of diabetes and its treatment.Loss of granuphilin and loss of syntaxin-1A cause differential effects on insulin granule docking and fusion.Interplay between Rab27a effectors in pancreatic β-cells.Granule mobility, fusion frequency and insulin secretion are differentially affected by insulinotropic stimuli.Observer-independent quantification of insulin granule exocytosis and pre-exocytotic mobility by TIRF microscopy.Activated Cdc42-bound IQGAP1 determines the cellular endocytic site Age-dependent labeling and imaging of insulin secretory granules.Syntaxin-3 regulates newcomer insulin granule exocytosis and compound fusion in pancreatic beta cells.MyRIP interaction with MyoVa on secretory granules is controlled by the cAMP-PKA pathway.Mathematical modeling of insulin secretion and the role of glucose-dependent mobilization, docking, priming and fusion of insulin granules.Insulinotropic effect of high potassium concentration beyond plasma membrane depolarization.Age-dependent preferential dense-core vesicle exocytosis in neuroendocrine cells revealed by newly developed monomeric fluorescent timer protein.Metabolic amplifying pathway increases both phases of insulin secretion independently of beta-cell actin microfilaments.

P2860

Q26866150-7EC77D41-274F-44FC-ADAB-391DE08CBE11 Q27322749-2E3ED76F-6A87-4E87-9667-7CBF3C45FBA1 Q27324203-0F6E4668-78D7-4BDE-94D3-2723BA950E61 Q28484639-7DBC4EF3-A9A0-4A3C-97F0-77EED9C7919B Q28578639-B409F5BD-F116-4C63-89C0-A7455D7D2507 Q30500213-04A00BA6-1182-4817-83CA-78C47470E1F0 Q30534507-812D65FD-73D6-4559-95A9-58046F344125 Q30541508-012DDE04-A5EE-426B-86C3-486152139F4F Q30622811-3BEDEF61-B034-41B7-8716-1C2D5B67FF7E Q33683217-9C028E8E-5BB2-4505-ADB1-EA5D023CE2A3 Q33779672-9AFDEAE3-1783-43B9-898C-E1CFC31D7313 Q34272586-7CAD8003-CDF4-43E8-B9E6-3893DE70A2F3 Q34775903-690CFA8D-CC4A-4ACF-9853-FAE069AD5287 Q35015726-6D4C1A40-4EBE-4D4F-AF10-AE8E70E8A2BD Q35170046-2CDB9BB0-0414-4DAE-8A70-1B0088D3FA2F Q35221742-E41EF53B-5D41-40E5-9C66-9538461FCD34 Q35630344-336964C3-8139-4A80-A9BB-D0B3CDC8F523 Q35870869-D822A39C-23C1-4A77-B536-36A517EE8FC4 Q35897574-5EA255EC-EAA3-4D54-BEAB-A3FD558ECAF4 Q36041923-0ABD2463-488B-454B-A761-B1417CC8C6C7 Q36132747-1654017F-D83E-4248-A6CE-D759ED521F6B Q37070824-3C27F339-CF0A-4325-A664-9BA357A62B31 Q37182979-533DA170-2CEF-4B2F-BD47-DEA1E9DD0AA1 Q37201909-B1D25B79-4D4F-44E5-9DBB-D350AE38B08B Q37247487-DEF53C7D-EA07-43BE-A227-76D2F2083207 Q37417286-3A70C3C1-503A-4518-A687-AD9991700975 Q37741935-BCF984BA-612D-40D9-9D9F-9F357DFC3CF5 Q37765396-78F29485-F219-49C6-8C8F-750DD7CDC07A Q38420628-654AAA73-978D-4ACD-BA62-1AC136E0CA49 Q38432549-E6211555-73F4-4C31-ACFC-0EA482D169C0 Q38917136-5993C0EA-A2E6-473E-BA9D-663BC166B80A Q39063198-F5124C4D-DF05-4CED-937F-834A53DD411D Q39085232-6F9E35CD-6CF1-498B-8868-C06D318CE2C2 Q39113094-DBB91D41-9E6D-4E98-ACFA-68D2C8D693A0 Q39248592-54A4F00E-F960-4AF3-B7C4-EA555C02E02A Q41198213-787C9F72-2F0C-49A8-A05D-3280F6691E53 Q41846065-03817900-BB41-4AD6-951A-46F876BAD85C Q42452912-D5E7228C-E97B-4E04-B5D6-A55C4C271F2C Q42943308-FE86A2DF-19FA-43FE-8517-A42991EE14EC Q43059442-C5205620-EC85-48DC-B048-A7E1BC36D5C5

P2860

Docking is not a prerequisite but a temporal constraint for fusion of secretory granules.

http://www.wikidata.org/entity/Q46657374

description

2008 nî lūn-bûn

@nan

2008年の論文

@ja

2008年学术文章

@wuu

2008年学术文章

@zh

2008年学术文章

@zh-cn

2008年学术文章

@zh-hans

2008年学术文章

@zh-my

2008年学术文章

@zh-sg

2008年學術文章

@yue

2008年學術文章

@zh-hant

name

Docking is not a prerequisite but a temporal constraint for fusion of secretory granules.

@en

Docking is not a prerequisite but a temporal constraint for fusion of secretory granules.

@nl

type

label

Docking is not a prerequisite but a temporal constraint for fusion of secretory granules.

@en

Docking is not a prerequisite but a temporal constraint for fusion of secretory granules.

@nl

prefLabel

Docking is not a prerequisite but a temporal constraint for fusion of secretory granules.

@en

Docking is not a prerequisite but a temporal constraint for fusion of secretory granules.

@nl

P1433

Q46657374-1A555BAF-D765-4C7B-9017-9AF085390E70

P1476

Q46657374-C43D417E-F21F-41D2-9153-4E91A2246694

P2093

Q46657374-0795465A-A5C4-4280-A344-4829A27F84D8

Q46657374-20E3D6B9-C5C2-4D41-B095-302769D78B97

Q46657374-AE8D30C9-5F9E-4AF5-874C-5A56B168DA42

Q46657374-B1DE3DD2-244D-4FC1-8F56-42D06832044B

P2860

Q46657374-0E362233-B44B-49D4-9F98-68699D912A5B

Q46657374-1D94EEF7-F5CC-4539-8DC2-8672844DB6C0

Q46657374-2E4D21B0-245D-41F4-B690-88B10AF6B49C

Q46657374-30786DA0-9FE6-4769-BFD4-91FC18DBC584

Q46657374-32D67B40-46BA-4C74-A11A-ECC986FE548A

Q46657374-339FC417-5C06-4931-AA43-369BE612FE34

Q46657374-3C6ECF6E-23D9-4E78-8A88-777F7EEC5365

Q46657374-5D52FBE6-4015-43DA-B9AA-3276AABD0F60

Q46657374-6DAEBA1A-E415-4EBF-84F4-EE529F9532E6

Q46657374-765F4A66-1826-4356-A092-5B518FCA423D

P304

Q46657374-170AE59A-4669-4435-B7BF-0FBB9CF675F6

P31

Q46657374-7A2BD22A-4DDA-49D1-A9C6-0D1C66206C65

P356

Q46657374-E0CC9E5A-CA2C-4AC1-BE0E-D3D900B8C30D

P433

Q46657374-EA2500B0-C41B-40E7-A700-DB879B0D3E2D

P478

Q46657374-9D264CBF-C1DA-4181-A0C5-50CA365B0A70

P577

Q46657374-EEB523AE-943B-45BA-98C7-B2592771EFED

P5875

Q46657374-7D289287-8ADA-483F-9E07-60EE93120563

P698

Q46657374-3D1EF5EB-8AFB-4160-A96A-B30C3776B389

P356

J.1600-0854.2008.00744.X

P1433

P1476

Docking is not a prerequisite but a temporal constraint for fusion of secretory granules.

@en

P2093

Hiroshi Gomi

http://www.w3.org/2001/XMLSchema#string

Kazuo Kasai

http://www.w3.org/2001/XMLSchema#string

Takuji Fujita

http://www.w3.org/2001/XMLSchema#string

Tetsuro Izumi

http://www.w3.org/2001/XMLSchema#string

P2860

Granuphilin modulates the exocytosis of secretory granules through interaction with syntaxin 1a

The Rab27a/granuphilin complex regulates the exocytosis of insulin-containing dense-core granules

Mutations in Mlph, encoding a member of the Rab effector family, cause the melanosome transport defects observed in leaden mice

Identification of an organelle receptor for myosin-Va

Novel rabphilin-3-like protein associates with insulin-containing granules in pancreatic beta cells

A mutation in Rab27a causes the vesicle transport defects observed in ashen mice

Fast insulin secretion reflects exocytosis of docked granules in mouse pancreatic B-cells.

Direct measurement of the evanescent field profile produced by objective-based total internal reflection fluorescence.

Comparative biology of Ca2+-dependent exocytosis: implications of kinetic diversity for secretory function.

Pancreatic beta-cell protein granuphilin binds Rab3 and Munc-18 and controls exocytosis.

P304

1191-1203

http://www.w3.org/2001/XMLSchema#string

P31

scholarly article

P356

10.1111/J.1600-0854.2008.00744.X

http://www.w3.org/2001/XMLSchema#string

P433

7

http://www.w3.org/2001/XMLSchema#string

P478

9

http://www.w3.org/2001/XMLSchema#string

P577

2008-04-04T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P5875

5456045

http://www.w3.org/2001/XMLSchema#string

P698

18397364

http://www.w3.org/2001/XMLSchema#string