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5′ AMP - activated protein kinase activationcausesGLUT4 translocation
Winder19995′ AMP - activated protein kinase activationcausesGLUT4 translocation
a signal cascadecan causeGLUT4 translocation
insulin and exercise(passive) is triggered byGLUT4 translocation
7/685 ) 5 ' AMP - activated protein kinase activationcausesGLUT4 translocation
a distal signal in the insulin - signaling cascadepreventsGLUT4 translocation
Aug;48(8):1667 - 71.5 ' AMP - activated protein kinase activationcausesGLUT4 translocation
American Journal of Physiology251E65–E70.)| false Kurth - KraczekEJHirshmanMFGoodyearLJWinderWW19995′ AMP - activated protein kinase activationcausesGLUT4 translocation
Many factors can act on intermediates of the insulin signal transduction pathwayto influenceGlut4 translocation
Kurth - Kraczek EJ , Hirshman MF , Goodyear LJ , Winder WW.5 ' AMP - activated protein kinase activationcausesGLUT4 translocation
Exposure of cultured cells to extracellular alkalosis ( pH 8.0 , 40 mM HCO3−triggeredVHA translocation
Kurth - Kraczek , EJ , Hirshman , MF , Goodyear , LJ & Winder , WW ( 1999 ) 5 ' AMP - activated protein kinase activationcausesGLUT4 translocation
GRF , GHRP-2 or PMA(passive) caused byPKC translocation
high insulin and glucose using 3T3-L1 adipocytes(passive) caused byGLUT4 translocation
up ... light - activated rhodopsin via an choice G - protein - coupled cascade that utilizes PLC and PKC and it is parallel towards the visible transduction cascade(passive) is set ... byarrestin translocation
both TCR and non - TCR signaling pathways in CTLs(passive) can be triggered bycentrosome translocation
KTRs shuttle between the nucleus and the cytoplasm , nuclear export and import ratescan influenceKTR translocation
events that would be predictedto triggerCRTC1 translocation
t - BHPcausedtranslocation of calpain
capacityto triggerarrestin translocation
the loss of both of them(passive) caused byGLUT4 translocation
the activation of PINK1–Parkin activity upon depolarization of mitochondria(passive) is triggered byp97 translocation
BAG6 depletion(passive) caused byGLUT4 translocation
blockage of the V2R(passive) could be prevented byAQP2 translocation
Fluid shear at 1 dyn / cm2causesAQP2 translocation
an AS160 mutant in which four of the Akt phosphorylation sites are mutated to Ala ( AS160–4P ) with putative constitutively active Rab - GAP activity ( 11(passive) caused byGLUT4 translocation
increases Rab - GTP activityto triggerGLUT4 translocation
that IRF8 directly interacts with NFATc1to preventNFATc1 translocation
this foreign protein may overwhelm the systempreventingGLUT4 translocation
activation of this pathway ... sufficientto causeGLUT4 translocation
either less fragmentation ( discontinuity ) during resorption or better fragment coverageto preventintraluminal translocation
endogenous calcium signalscan triggerCaMKII translocation
preventing actin dynamicscan preventGLUT4 translocation
increased Serum RBP4 levels , and/or(passive) potentially caused byGLUT-4 translocation
a tubulin code that involves multiple PTMs ( Verhey and Gaertig , 2007(passive) is influenced bykinesin translocation
ER Ca2 + depletion(passive) triggered bySTIM1 translocation
H2Ocausedtranslocation of NF‐κB
either hormone(passive) caused byGLUT4 translocation
nocodazole(passive) caused byEGR-1 translocation
the membranescausingglut4 translocation
Down syndrome(passive) caused byDown syndrome
to glucose uptake [ 18contributesto glucose uptake [ 18
in insulin - independent glucose uptakeresultingin insulin - independent glucose uptake
to hyperglycemia and systemic insulin resistanceleadingto hyperglycemia and systemic insulin resistance
in increased glucose uptake and glycogen synthesisresultingin increased glucose uptake and glycogen synthesis
in trisomy for chromosome 13qresultingin trisomy for chromosome 13q
of homologous chromosomes 21q;21q and reproductive risk found in the family affected by this type oftranslocationcomposedof homologous chromosomes 21q;21q and reproductive risk found in the family affected by this type oftranslocation
to the high rates of ATP hydrolysis we have observed in the current studyis ... contributingto the high rates of ATP hydrolysis we have observed in the current study
to glucose transport [ 27leadingto glucose transport [ 27
to the production of the E2A / PBX1 fusion transcriptleadingto the production of the E2A / PBX1 fusion transcript
to BCAM - AKT2 fusionleadingto BCAM - AKT2 fusion
up at a threshold where around 3 % of the full total substances of rhodopsin are bleachedis setup at a threshold where around 3 % of the full total substances of rhodopsin are bleached
The changes of chromosome number and karyotype are suggested(passive) to be caused byThe changes of chromosome number and karyotype are suggested
from fusion of the E2A gene ( also called TCF3 ) in the 19p13 site with the PBX1 gene on the 1q23 site results in the formation of a chimeric transcription factor which in turn causes an abnormal activation and dysfunction of the homeobox gene ( PBX1 ) , which leads to transactivation of various genes , and finally a malignant cell phenotype.16 Experimental studies have shown that E2A- PBX1 gene rearrangement initially causes a blockage of normal cell differentiation of myeloid progenitors and paradoxically induces apoptosis in the Pre - B cell linesresultingfrom fusion of the E2A gene ( also called TCF3 ) in the 19p13 site with the PBX1 gene on the 1q23 site results in the formation of a chimeric transcription factor which in turn causes an abnormal activation and dysfunction of the homeobox gene ( PBX1 ) , which leads to transactivation of various genes , and finally a malignant cell phenotype.16 Experimental studies have shown that E2A- PBX1 gene rearrangement initially causes a blockage of normal cell differentiation of myeloid progenitors and paradoxically induces apoptosis in the Pre - B cell lines
part(passive) caused bypart
the TTFLcould influencethe TTFL
in a chromosome with two centromeres which can behave as a single centromerecan resultin a chromosome with two centromeres which can behave as a single centromere
in the SYT - SSX fusion transcriptresultingin the SYT - SSX fusion transcript
membrane stiffness(passive) caused bymembrane stiffness
in partial trisomy 2presultingin partial trisomy 2p
terminalBcell differentiationpreventsterminalBcell differentiation
downstream from phototransduction In the final set of experimentsis triggereddownstream from phototransduction In the final set of experiments
the immobilisation of passing AMPARtriggeredthe immobilisation of passing AMPAR
to activation of Orai1 and the subsequent calcium influx into astrocytesleadingto activation of Orai1 and the subsequent calcium influx into astrocytes
in the ASPACR1-TFE3 fusion proteinresultingin the ASPACR1-TFE3 fusion protein
at a critical threshold of light intensity by a specific signaling mechanismis triggeredat a critical threshold of light intensity by a specific signaling mechanism
as light intensity reaches a critical threshold To quantify the subcellular distribution of arrestin in the dark and the light dependence of its translocationis triggeredas light intensity reaches a critical threshold To quantify the subcellular distribution of arrestin in the dark and the light dependence of its translocation
from the elevation of [ cAMP]iresultingfrom the elevation of [ cAMP]i
to the development of specific lymphoma subtypescontributesto the development of specific lymphoma subtypes
in the PML / RARA fusion generesultingin the PML / RARA fusion gene
to leukemic transformationcontributesto leukemic transformation
to a fusion gene that expresses truncated ETV1 ( dETV1 ) , or to overexpression of the wild - type ETV1genecan leadto a fusion gene that expresses truncated ETV1 ( dETV1 ) , or to overexpression of the wild - type ETV1gene
primary cilium signaling defects , ciliary instability and ciliopathies in human and mousecauseprimary cilium signaling defects , ciliary instability and ciliopathies in human and mouse
to the Philadelphia ( Ph ) chromosomeleadsto the Philadelphia ( Ph ) chromosome
as a result of motor activitycan resultas a result of motor activity
cell cycle arrest at G2 / M phase and induced apoptosiscausingcell cycle arrest at G2 / M phase and induced apoptosis
so prior specific immuno - monotherapy with easy - to - understand information on influenza cross - react against osteoporosiscausesso prior specific immuno - monotherapy with easy - to - understand information on influenza cross - react against osteoporosis
up with a G - protein - coupled cascade through PLC and PKC signalingis setup with a G - protein - coupled cascade through PLC and PKC signaling
cell cycle arrest at G2 / M phase and induces apoptosis of breast cancer cellscausingcell cycle arrest at G2 / M phase and induces apoptosis of breast cancer cells
to the activation of glycogen synthase [ 31 , 41 , 42leadingto the activation of glycogen synthase [ 31 , 41 , 42