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Preferentially catalyzes the dephosphorylation of 'Ser- 5' within the tandem 7 residues repeats in the C-terminal domain (CTD) of the largest RNA polymerase II subunit POLR2A. Additionally we are shipping GIP Kits (57) and GIP Proteins (8) and many more products for this protein.
Showing 10 out of 85 products:
Human Polyclonal GIP Primary Antibody for IHC (fro), IF - ABIN115738
Portela-Gomes, Stridsberg, Johansson, Grimelius: Complex co-localization of chromogranins and neurohormones in the human gastrointestinal tract. in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 1997
Human Polyclonal GIP Primary Antibody for IHC, ELISA - ABIN1584506
Chang, Cai, Lo, Amigo, Park, Hsu: Adaptive selection of an incretin gene in Eurasian populations. in Genome research 2011
The loss of food-induced GIP response in Roux-limb of intestine likely contributes to the attenuated serum GIP response to feeding.
GIP induces the expression of the proatherogenic cytokine osteopontin (OPN) in mouse arteries via local release of endothelin-1 and activation of CREB. GIPR mRNA is higher in symptomatic carotid endarterectomy patients.
These studies support the hypothesis that a reduction in GIP signaling using a GIP-neutralizing mAb might provide a useful method for the treatment and prevention of obesity and related disorders.
This study provides evidences that GIP acts directly on osteoblasts and is capable of improving collagen maturity and fibril diameter.
There was decrease in GIP gene transcripts and protein in the gut (show GUSB Antibodies) of HNF1a (show HNF1A Antibodies)-null mice.
The patterns of colocalisation of the K cell marker, glucagon-like insulinotropic peptide, and the L cell markers, glucagon like peptide-1 and peptide YY, in enteroendocrine cells of the small intestine and colon of mouse and pig, were investigated.
These data indicate that GLP-1 (show GCG Antibodies) but not GIP is a key mediator of beta cell mass expansion and related adaptations in pregnancy, triggered in part by generation of intra-islet GLP-1 (show GCG Antibodies).
NUCB2/nesfatin-1 (show NUCB2 Antibodies) is co-localized with GLP-1 (show GCG Antibodies) and GIP in small intestinal cells. Data support the hypothesis that nesfatin-1 (show NUCB2 Antibodies) is present in enteroendocrine cells and that it stimulates incretin secretion.
Circulating levels of GIP were significantly decreased in FABP5 (show FABP5 Antibodies)-deficient mice.
phosphatidylinositol 3-kinase gamma has a role in insulin (show INS Antibodies) secretion induced by glucose-dependent insulinotropic polypeptide
Our results might indicate an altered DPP4 (show DPP4 Antibodies)-incretin system and altered immunoregulation including a potentially dysfunctional GLP1 (show GCG Antibodies)(9)(-)(36) signaling in T1DM.
Fasting GIP concentrations are higher in individuals with a history of cardiovascular disease (myocardial infarction, stroke) when compared with control subjects.
Data suggest that high levels of blood glucose or AGEs (advanced glycation end products), as seen in hyperglycemia, reduce secretion of insulin (show INS Antibodies) by pancreatic beta cells via antagonism of GIP (gastric inhibitory polypeptide)/GIP receptor signaling.
Data confirm that postprandial plasma levels of glucose-dependent insulinotropic polypeptide (GIP) and insulin (INS (show INS Antibodies)) are responsive to glycemic index of foods consumed; glycemic index of breakfast cereals regulate plasma postprandial GIP and INS (show INS Antibodies).
irisin (show FNDC5 Antibodies) and GIP might contribute to the development of polycystic ovary syndrome and may also represent novel polycystic ovary syndrome biomarkers
Data suggest that postprandial blood levels of both GIP and insulin (show INS Antibodies) can be regulated by diet; here, inclusion of nopal/Opuntia/cactus (show SLC25A20 Antibodies) (a functional food in traditional Mexican medicine) in breakfast reduces postprandial levels of GIP and insulin (show INS Antibodies).
These novel results support the notion that the GIP-GIPR (show GIPR Antibodies) axis plays a role in the etiology of central obesity in humans
Data from studies in healthy Japanese men suggest that plasma GIP levels in postprandial period are dose dependently increased by fat content of meals of ordinary size, despite the amount of additional fat being relatively small.
Dietary fructose elicits GLP-1 (show GCG Antibodies) secretion without simultaneous release of glucagonotropic GIP.
porcine GIP stimulated the proliferation of MC-26 cells, a mouse CRC (show RYR1 Antibodies) cell line, in a concentration-dependent manner.
Preferentially catalyzes the dephosphorylation of 'Ser- 5' within the tandem 7 residues repeats in the C-terminal domain (CTD) of the largest RNA polymerase II subunit POLR2A. Negatively regulates RNA polymerase II transcription, possibly by controlling the transition from initiation/capping to processive transcript elongation (By similarity). Recruited by REST to neuronal genes that contain RE-1 elements, leading to neuronal gene silencing in non-neuronal cells.
gasdermin domain containing 1
, gasdermin domain-containing protein 1
, gastric inhibitory polypeptide
, glucose-dependent insulinotropic polypeptide
, NLI-interacting factor 3
, carboxy-terminal domain RNA polymerase II polypeptide A small phosphatase 1
, golli-interacting protein
, nuclear LIM interactor-interacting factor 3
, small C-terminal domain phosphatase 1
, small CTD phosphatase 1
, incretin hormone
, Glucose-dependent insulinotropic peptide