GRPP (human) Formula C136H215N41O58S Sequence Arg_Ser_Leu_Gln_Asp_Thr_Glu_Glu_Lys_Ser_Arg_Ser_Phe_Ser_Ala_Ser_Gln_Ala_Asp_Pro_Leu_Ser_Asp_Pro_Asp_Gln_Met_Asn_Glu_Asp
- Known as:
- GRPP (H. sapiens) Formula C136H215N41O58S Sequence Arg_Ser_Leu_Gln_Asp_Thr_Glu_Glu_Lys_Ser_Arg_Ser_Phe_Ser_Ala_Ser_Gln_Ala_Asp_Pro_Leu_Ser_Asp_Pro_Asp_Gln_Met_Asn_Glu_Asp
- Catalog number:
- 89073
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- GLSChina
- Gene target:
- GRPP (human) Formula C136H215N41O58S Sequence Arg_Ser_Leu_Gln_Asp_Thr_Glu_Glu_Lys_Ser_Arg_Ser_Phe_Ser_Ala_Ser_Gln_Ala_Asp_Pro_Leu_Ser_Asp_Pro_Asp_Gln_Met_Asn_Glu_Asp
Related genes to: GRPP (human) Formula C136H215N41O58S Sequence Arg_Ser_Leu_Gln_Asp_Thr_Glu_Glu_Lys_Ser_Arg_Ser_Phe_Ser_Ala_Ser_Gln_Ala_Asp_Pro_Leu_Ser_Asp_Pro_Asp_Gln_Met_Asn_Glu_Asp
- Gene:
- GCG NIH gene
- Name:
- glucagon
- Previous symbol:
- -
- Synonyms:
- GLP1, GLP2, GRPP, GLP-1
- Chromosome:
- 2q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2017-02-07
Related products to: GRPP (human) Formula C136H215N41O58S Sequence Arg_Ser_Leu_Gln_Asp_Thr_Glu_Glu_Lys_Ser_Arg_Ser_Phe_Ser_Ala_Ser_Gln_Ala_Asp_Pro_Leu_Ser_Asp_Pro_Asp_Gln_Met_Asn_Glu_Asp
Paliperidone N-Oxide CAS: 761460-08-6 Formula: C23H27FN4O4 2,4-Dibromo-17,17-ethylenedioxy-1,3,5(10)-estratriene-3,16α-diol CAS: 90474-20-7 Formula: C20H24Br2O4 2,4-Dibromo-17,17-ethylenedioxy-1,3,5(10)-estratriene-3-ol CAS: Formula: C20H24Br2O3 3,3',5,5'-Tetraiodo Thyroformic Acid CAS: 2055-97-2 Formula: C13H6I4O4 3,5,3',5'-Tetrachlorobisphenol A CAS: 79-95-8 Formula: C15H12Cl4O2 4-(2,6,6-Trimethyl-2-cyclohexen-1-ylidene)-2-acetoxybut-2-ene CAS: 61693-39-8 Formula: C15H22O2 4-Benzyloxy-1-cyclohexanecarbonitrile (cis / trans mixture) CAS: 95233-32-2 Formula: C14H17NO 5-[(4-Methoxyphenyl)-diphenylmethylamino-6-methoxy-9H-purin-9-yl]-13C2, 15N-3-(phenylmethoxy)-2-[(phenylmethoxy)methyl]-cyclopentanol CAS: Formula: 6-Phenylhexylamine Hydrochloride CAS: 120375-57-7 Formula: C12H20ClN Paliperidone-d4 CAS: 1020719-55-4 Formula: C23H23D4FN4O3 [Tyr63] PTH (63_84), human
Human ELC ELISA KIT 96 TEST
"Recombinant Human Carboxypeptidase E_CPE""Recombinant Human Carboxypeptidase E_CPE""Recombinant Human Carboxypeptidase E_CPE" Related articles to: GRPP (human) Formula C136H215N41O58S Sequence Arg_Ser_Leu_Gln_Asp_Thr_Glu_Glu_Lys_Ser_Arg_Ser_Phe_Ser_Ala_Ser_Gln_Ala_Asp_Pro_Leu_Ser_Asp_Pro_Asp_Gln_Met_Asn_Glu_Asp
- To determine whether genetic proxies for incretin pathway perturbation are associated with fracture risk and bone mineral density, providing human genetic evidence relevant to the skeletal safety of incretin-based therapies. - Source: PubMed
Publication date: 2026/09/29
Cheng WenjieLiu WeijieWei JieZeng ChaoLyu HouchenZhao Sizheng Steven - Pancreatic β-cell dedifferentiation is a pathological mechanism that contributes to β-cell dysfunction and loss during type 2 diabetes (T2D), but the underlying mechanisms remain incompletely understood. MicroRNAs (miRNAs) are key post-transcriptional regulators of cellular identity and function. We previously identified miR-483 as a β-cell-enriched miRNA that promotes β-cell function by targeting Aldh1a3. Here, we investigated its role under high-fat diet (HFD)/multiple low-dose streptozotocin (STZ)-induced metabolic stress. β-cell-specific miR-483 deficiency exacerbated hyperglycemia and impaired glucose tolerance, accompanied by increased ALDH1A3 expression and reduced insulin expression in GFP-labeled cells. Under HFD/STZ-induced metabolic stress, miR-483 deficiency also increased glucagon production and the abundance of GFP+GCG+ and ALDH1A3+GCG+ cells, consistent with loss of β-cell identity and emergence of α-cell-like characteristics. Single-cell RNA sequencing revealed increased β-cells heterogeneity, including a subpopulation with glucagon expression and an altered endocrine phenotype. In addition, miR-483 deficiency was associated with mitochondrial fragmentation, impaired respiratory function, and increased oxidative stress. Together, these findings suggest that miR-483-ALDH1A3 axis contributes to the coordination of β-cell identity with mitochondrial and metabolic homeostasis during metabolic stress. - Source: PubMed
Publication date: 2026/09/26
Matson KatyMacLeod AaronSempek EllieNoble JordanTapert BryceAlipour FarhadTang XiaohuMarceau AimeeSatin Leslie STang Xiaoqing - Nomex honeycomb core sandwich composites are attractive for lightweight structural applications because of their high specific stiffness. However, drilling required for mechanical joining can introduce both surface and subsurface damage and may change the mechanical and dynamic response of the structure. This study examines Nomex aramid honeycomb sandwich composites with C/C/C, C/G/C, G/C/G, and G/G/G face-sheet configurations using three-point bending, drilling, image analysis, ultrasonic C-scan, and acoustic impact measurements. The C/C/C configuration reached an average bending load 36.05% higher than G/G/G and reduced the entry and exit side delamination areas by 88.91% and 78.89%, respectively. Although C/C/C produced the highest thrust forces during drilling, it also showed the smallest surface and internal damage regions, indicating that thrust force alone does not fully describe hole quality. C/G/C also exhibited less damage than G/C/G; however, these two hybrid configurations differ in both carbon/glass content and ply position, so the contribution of each factor cannot be separated independently. After drilling, the natural frequency decreased, and the damping ratio increased in all configurations. Overall, the carbon-rich face sheets provided higher bending resistance and more effectively limited drilling-induced damage. - Source: PubMed
Publication date: 2026/09/10
Demirci Ibrahim - Diastase activity is a key international criterion for assessing honey quality, indicative of freshness and the absence of excessive heat treatment. This study found that the diastase activity of honey (TCH) was only 3.45, significantly lower than other 11 common honeys with range of 9.96 to 23.06. Furthermore, its diastase activity abnormally decreased during honey ripening. Flavonoids have been reported to effectively inhibit diastase activity. The underlying mechanisms were investigated in vitro and in vivo based on the characteristic flavonoids in TCH identified by LC-MS/MS, i.e. unique (-)-gallocatechin gallate (GCG) and high-content naringenin chalcone (NGC). In vitro enzymatic assays indicated that GCG and NGC inhibited -amylase activity via mixed-type. The binding of GCG and NGC on -amylase was further characterized by fluorescence quenching and molecular docking. In vivo studies revealed that dietary supplementation of GCG and NGC suppressed the gene expression in the hypopharyngeal glands of honey-ripening bees (15-day-old) by 78.92% and 67.71%, respectively, and in foragers (25-day-old) by 91.14% and 56.48%, respectively. Network pharmacology analysis linked this suppression by interfering with four α-amylase-related pathways. - Source: PubMed
Publication date: 2026/09/12
Jiang HuizhiLi ZhenXu TianyuXu MinChen WeixuanHe ShengyangWu XiaoboYan WeiyuZhang QingfengZeng Zhijiang - Influenza remains a significant global public health threat, causing substantial morbidity and mortality worldwide. While vaccination serves as the best preventive strategy, considerable interindividual variability in vaccine-induced immune responses persists. The rs2281929 polymorphism (c.A31G; p.T11A; ACG>GCG), which corresponds to the evolutionarily conserved mouse mutation (c.A31G; ACT>GCT), has been associated with enhanced antibody responses to influenza vaccination in humans, though its functional mechanisms remain unknown. This study aimed to investigate how this mutation affects influenza vaccine immunogenicity using a knock-in mouse model. A knock-in mouse model was generated using CRISPR/Cas9 technology. Homozygous (HO) and wild-type (WT) mice were immunized with a quadrivalent influenza vaccine in a prime-boost regimen. Humoral immune responses were assessed by Enzyme-linked immunosorbent assay, hemagglutination inhibition (HI), and microneutralization (MN) assays. Antibody-secreting cells (ASCs) were quantified by Enzyme-linked immunospot assays. Germinal center B cells, plasma cells, plasmablast cells, conventional dendritic cell (cDC) subsets, and T helper (Th) cells were analyzed by flow cytometry. Statistical comparisons were performed using a two-sample -test. The mutation did not alter Zbtb46 protein expression or its abundance in cDCs. Following vaccination, HO mice exhibited significantly enhanced humoral responses, including higher HA-specific IgG titers, HI and MN antibody levels, and increased numbers of ASCs. Flow cytometry revealed elevated proportions of germinal center B cells and plasma cells in HO mice. Furthermore, HO mice showed a selective expansion of type 1 cDCs (cDC1s) and a concomitant increase in Th1 cell frequencies and IFN-γ-secreting cells, while cDC2 proportions and Th2 responses remained unchanged. The mutation is associated with enhanced influenza vaccine immunogenicity, concomitant with increased cDC1 proportions, Th1 polarization, and germinal center-dependent humoral immunity. These observed associations suggest a candidate mechanism whereby modulation may shape adaptive immunity, though further functional studies are required to establish causality. These findings provide insights into host genetic variation in vaccine responsiveness and may inform personalized vaccination strategies. - Source: PubMed
Publication date: 2026/09/06
Zhao YifanLei YuxuanXu QiuyiZhang ShumiaoXie QianYuan LifangLiang RuiqiWen SiminShu Yuelong