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anti-Human Insulin Anticorps:
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Buffalo (Bubalus) Polyclonal Insulin Primary Antibody pour IEM, ICC - ABIN617877
Tay, Wong: Insulin-like immunoreactivity in the monkey spinal cord. dans Acta anatomica 1992
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Human Monoclonal Insulin Primary Antibody pour IHC (p) - ABIN3043651
Han, Qiu, Zhang, Kong, Wang, Wang, Li, Duan, Wang, Song, Wang: Transplantation of sertoli-islet cell aggregates formed by microgravity: prolonged survival in diabetic rats. dans Experimental biology and medicine (Maywood, N.J.) 2009
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Cow (Bovine) Monoclonal Insulin Primary Antibody pour CyTOF, FACS - ABIN4900790
Cucak, Grunnet, Rosendahl: Accumulation of M1-like macrophages in type 2 diabetic islets is followed by a systemic shift in macrophage polarization. dans Journal of leukocyte biology 2014
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Human Polyclonal Insulin Primary Antibody pour EIA, FACS - ABIN372838
Madsen, Knauf, Gotfredsen, Pilling, Sjögren, Andersen, Andersen, de Boer, Manova, Barlas, Vundavalli, Nyborg, Knudsen, Moelck, Fagin: GLP-1 receptor agonists and the thyroid: C-cell effects in mice are mediated via the GLP-1 receptor and not associated with RET activation. dans Endocrinology 2012
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Cow (Bovine) Monoclonal Insulin Primary Antibody pour FACS - ABIN4898619
Kalis, Bolmeson, Esguerra, Gupta, Edlund, Tormo-Badia, Speidel, Holmberg, Mayans, Khoo, Wendt, Eliasson, Cilio: Beta-cell specific deletion of Dicer1 leads to defective insulin secretion and diabetes mellitus. dans PLoS ONE 2012
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Human Polyclonal Insulin Primary Antibody pour IHC, IHC (p) - ABIN4326017
Lindskog, Asplund, Engkvist, Uhlen, Korsgren, Ponten: Antibody-based proteomics for discovery and exploration of proteins expressed in pancreatic islets. dans Discovery medicine 2010
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Human Monoclonal Insulin Primary Antibody pour ELISA (Capture), ELISA - ABIN617624
Back, Scheuner, Han, Song, Ribick, Wang, Gildersleeve, Pennathur, Kaufman: Translation attenuation through eIF2alpha phosphorylation prevents oxidative stress and maintains the differentiated state in beta cells. dans Cell metabolism 2009
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Human Monoclonal Insulin Primary Antibody pour ELISA (Capture), ELISA - ABIN617623
Kojima, Fujimiya, Matsumura, Nakahara, Hara, Chan: Extrapancreatic insulin-producing cells in multiple organs in diabetes. dans Proceedings of the National Academy of Sciences of the United States of America 2004
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Data suggest that higher plasma levels of ceramide with saturated fatty acid are associated with higher fasting levels of insulin and insulin resistance; in contrast, higher levels of sphingomyelin with saturated fatty acid are associated with lower fasting insulin and insulin resistance; this study was conduced in American Indians in AZ, OK, SD, and ND.
in latent autoimmune diabetes in adults, higher leptin (Montrer LEP Anticorps) secretion may exert a direct effect on beta cell function leading to more insulin sensitivity
Identify a novel proinsulin-associated locus and demonstrate that whilst proinsulin levels are associated with carotid intima media thickness measures, proinsulin per se is unlikely to have a causative effect on cIMT.
Data suggest that both a KATP channel-dependent triggering pathway (that induces a [Ca2 (Montrer CA2 Anticorps)+]i rise in beta-cells) and an amplifying pathway (that augments the effect of Ca2 (Montrer CA2 Anticorps)+ on exocytosis) are crucial for control of insulin secretion in human islets; these studies used cultured pancreatic islets from multiorgan donors exposed to a variety of pharmacological agents.
In the present study, the protein inhibitor of activated STAT (Montrer STAT1 Anticorps) Y (PIASy (Montrer PIAS4 Anticorps)) was identified as a novel Isl1 (Montrer ISL1 Anticorps)-interacting protein. Furthermore, PIASy (Montrer PIAS4 Anticorps) and Isl1 (Montrer ISL1 Anticorps) upregulate insulin gene expression and insulin secretion in a dose-dependent manner by activating the insulin promoter.
Muscle-related indices positively correlated with C-peptide, which showed endogenous insulin reserve
Data suggest that corticosterone and cortisol suppress voltage-dependent Ca2+ channel function and Ca2+ fluxes in beta-cells; however, insulin secretion, maximal ATP/ADP responses to glucose, and beta-cell identity/differentiation are all unaffected by these glucocorticoids.
In long-standing models, glucose is viewed as a primary stimulator of insulin secretion; recent models postulate that glucose activates a cell-surface receptor, namely the glucose-sensing receptor, on insulin-secreting cells. [REVIEW]
Data suggest that beta-cell insulin secretory granules, unlike neuronal synaptic vesicles, exhibit biphasic secretory mechanism that requires additional distinct features in exocytosis; beta-cell insulin exocytotic events appear to be mediated by Munc18/SNARE (Montrer NAPA Anticorps) protein complexes distinct from those involved in predocking/fusion of insulin secretory granules with plasma membrane. [REVIEW]
Data suggest that glucose-stimulated insulin secretion involves interplay between metabolic and cationic events involving small G-proteins; activation of these signaling proteins promotes cytoskeletal remodeling, transport and docking of insulin granules on the plasma membrane for exocytotic secretion of insulin. [REVIEW]
Study used well-tempered bias exchange metadynamics simulations to determine the equilibrium ensembles of an insulin molecule under amyloidogenic conditions of low pH and high temperature. The folded state of a single insulin molecule was shown to be the most stable, longest-lived state even under amyloidogenic conditions.
The findings are consistent with previous studies that indicate a link between Na,K-ATPase (Montrer ATP1A1 Anticorps) activity and SFK signaling.
PTPLAD1 (Montrer PTPLAD1 Anticorps) and AMPK (Montrer PRKAA1 Anticorps) are rapidly compartmentalized within the plasma membrane (PM) and Golgi/endosome fractions after insulin stimulation and that ATIC (Montrer ATIC Anticorps) later accumulates in the Golgi/endosome fraction.
Pdx-1 (Montrer PDX1 Anticorps), MafA (Montrer MAFA Anticorps) and NeuroD1 (Montrer NEUROD1 Anticorps) bind to the A, C and E elements in the insulin promoter and regulate the transcriptional activity of the insulin promoter.
The interplay of the adiponectin system, TNFalpha (Montrer TNF Anticorps) and insulin at a transcriptional level and, their effects on the adipogenic transcription factor PPARgamma (Montrer PPARG Anticorps), as well as on the activation of main insulin signaling pathways, is reported.
Thermodynamics of insulin unfolding have been quantified by differential scanning calorimetry and thermal unfolding measurements to determine the extent and nature of their stabilization of the insulin hexamer.
Exposing the hydrophobic core of insulin can induce the increase of amyloidogenicity and formation of higher-order polymerized fibrils, which is less toxic to membranes.
Data suggest that a mutation in INS (C94Y) results a transgenic disease model for the investigation of permanent neonatal diabetes.
The results show that modulation of plasma insulin levels by dietary carbohydrates seems possible in anabolic sows, but IGF-I (Montrer IGF1 Anticorps) levels are less easily modified.
insulin increased GCLc (Montrer GCLC Anticorps) promoter activity, which required a prerequisite increase or decrease in medium glucose
The structural dynamics of insulin hexamer dissociation were studied by the photoinduced temperature jump technique and monitored by time-resolved X-ray scattering. The process of hexamer dissociation was found to involve several transient intermediates, including an expanded hexamer and an unstable tetramer.
Insulin signaling role in skeletal muscle atrophy and autophagy in in transition and postpartum period
Differences between human and bovine insulin kinetics under shear
increased sensitivity to glucose clearance and skeletal muscle insulin signaling during dietary restriction
Hormonal gene expression involved in residual feed intake in dairy cows may be related to the molecular regulation of the leptin (Montrer LEP Anticorps)-NPY (Montrer NPY Anticorps) and insulin signaling pathways.
Raman spectra of amino acids by Density Functional Theory method have been calculated. Experimental Raman spectra of insulin has been done. The simulated Raman spectrum of insulin is obtained from amino acid spectrum.
Contains Binding kinetics for insulin binding
Using synchrotron radiation (SR), the crystal structures of T6 bovine insulin complexed with Ni(2 (Montrer VMP1 Anticorps)+) and Cu(2+) were solved to 1.50 and 1.45 A resolution, respectively.
The present study examined the effect of insulin-mediated activation of the mammalian target of rapamycin (Montrer FRAP1 Anticorps) complex 1 (MTORC1) signaling network on the proliferation of primary culture of theca-interstitial (T-I) cells.
insulin supports early initiation of the mesodermal factor Brachyury (Montrer TBX1 Anticorps) and the signalling molecules Wnt3a (Montrer WNT3A Anticorps) and Wnt4 (Montrer WNT4 Anticorps) as well as the progression of mesoderm formation
Data show that type 1 diabetic blastocyst did not express insulin mRNA.
Data (including data from studies in knockout mice) suggest that Ins2 is involved in impaired nociception/diabetic neuropathy; here, mice heterozygous for mutant Ins2 exhibit (a) significant loss of intra-epidermal nerve fibers, (b) markedly reduced responsiveness to heat in dorsal root ganglion neurons, and (c) mostly unchanged function of cold-sensitive neurons; such mice become diabetic soon after weaning.
In the present study, the mRNA expression of the two mouse insulin genes Ins1 and Ins2 was investigated in MIN6 cells treated with different concentrations of melatonin, and insulin secretion was detected under the same conditions. Following the overexpression or silencing of MTNR1B (Montrer MTNR1B Anticorps), the activities of components of the MAPK (Montrer MAPK1 Anticorps) signaling pathway
These results suggest that PABP (Montrer EBP Anticorps) interacts with HuD (Montrer ELAVL4 Anticorps) in basal glucose conditions making translation inhibitory complex, however upon glucose stimulation this association is affected and PABP (Montrer EBP Anticorps) is acted upon by PDI (Montrer PDIA3 Anticorps) resulting in stimulation of insulin translation.
Data (including data from studies using knockout mice) suggest that Ins1 and Ins2 are required for pancreatic beta-cell maturation; thus, Ins1 and Ins2 are needed for normal beta-cell development and for maintenance of normal beta-cell function.
cTAGE5 (Montrer CTAGE5 Anticorps) deletion in pancreatic beta cells impairs proinsulin trafficking and insulin biogenesis in mice.
These results suggest that prolonged exposure to hyperglycemia in the Ins2(Akita+/-) mice leads to progressive testicular disruption mediated by testicular activin (Montrer Actbeta Anticorps) activity, rather than hormonal dysregulation.
report that EndMTs occur in the diabetic endothelium of Ins2Akita/wt mouse, and show that induction of sex determining region Y-box 2 (Sox2 (Montrer SOX2 Anticorps)) is a mediator of excess BMP signaling that results in activation of EndMTs and increased vascular calcification
Transplantation of transduced hematopoietic stem cells (HSCs) expressing proinsulin II prevents diabetes development.
Wnt3a increased the expression of NeuroD1 and Ins2 in the hypothalamus.
Data suggest that resveratrol acts on differentiating preadipocytes by inhibiting insulin signaling, mitochondrial biogenesis, and lipogenesis.
Temporal and spatial expression of two insulin genes (insa and insab) during early developmental stages.
These findings suggest that GHRL (Montrer GHRL Anticorps) regulates INS synthesis by mediating its action on growth hormone secretagogue-receptor (Montrer GHSR Anticorps) in the central nervous system and partly involved in carbohydrate-glycogen (Montrer GYS2 Anticorps) metabolism.
Our results indicate that in adult tilapia insulin expression is not restricted to the endocrine pancreatic cells, but also occurs in endocrine cells of the pituitary gland and in the neuronal cells of the brain.
After removal of the precursor signal peptide, proinsulin is post-translationally cleaved into three peptides: the B chain and A chain peptides, which are covalently linked via two disulfide bonds to form insulin, and C-peptide. Binding of insulin to the insulin receptor (INSR) stimulates glucose uptake. A multitude of mutant alleles with phenotypic effects have been identified. There is a read-through gene, INS-IGF2, which overlaps with this gene at the 5' region and with the IGF2 gene at the 3' region. Alternative splicing results in multiple transcript variants.