Mouse Anti-Bovine INS Hybridoma [DD0D21] (CSC-H1200)

This hybridoma produces mAbs (IgG1, kappa light chain) against bovine INS

General Information


Immunogen
Beef insulin
Isotype
IgG1, kappa light chain
Fusion Species
Mouse X Mouse Hybridoma
Immunological Donor
Mouse spleen
Myeloma
Sp2/0-Ag14
Clone
DD0D21
Cell Line Description
Animals were immunized with beef insulin. Spleen cells were fused with Sp2/0-Ag14 myeloma cells. The antibody binds insulin from human, cow, pig, rabbit, rat and sheep. The antibody also binds pro-insulin from chicken, pig and cow. The antibody binds guinea pig, and fish insulins poorly. Tested and found negative for ectromelia virus (mousepox).
Morphology
Lymphoblast
Growth Properties
Suspension

Culture Method


Complete Growth Medium
DMEM with 4 mM L-glutamine, 4500 mg/L glucose, 1 mM sodium pyruvate and 1500 mg/L sodium bicarbonate, supplemented with 10% FBS.
Subculturing
Incubate cells at 37°C with 5% CO2 in air atmosphere, renew medium every 2-3 days, start cells at 2x10^5 cells/mL and maintain cultures between 1x10^5-1x10^6 cells/ml
Storage
Liquid nitrogen vapor phase.

Target


Synonyms
INS;insulin;proinsulin;
Entrez Gene ID

Citations


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References


Sex-based trade-offs in the innate and acquired immune systems ofSternotherus minor

JOURNAL OF EXPERIMENTAL ZOOLOGY PART A-ECOLOGICAL AND INTEGRATIVE PHYSIOLOGY

Authors: Lopez-Perez, Jorge E.; Meylan, Peter A.; Goessling, Jeffrey M.

Longevity patterns in most vertebrates suggest that females benefit most from maintenance investment. A reversed longevity pattern in loggerhead musk turtles (Sternotherus minor) allowed us to test trade-offs between maintenance and survivorship. We tested the hypothesis that the sex with greater longevity has greater maintenance than the sex with shorter longevity. We also compared the following parameters between sexes: Bactericidal ability (BA) and heterophil:lymphocyte ratios (HLR). Baseline blood samples were collected from turtles in the field; a subset of turtles was returned to a laboratory for experiments of acquired immune responses to sheep red blood cells (SRBC). We found no support for the original hypothesis of reversal in sex-dependent immune trade-offs (difference between sex SRBC titers:p = .102; interaction between treatment and sex:p = .177; difference between treatments:p < .001; effect of sex on BA:p = .830; effect of sex on HLR:p = .717). However, we did find support for sex-dependent differences in immunity in the relationship between HLR and body condition (BCI) (effect of BCI on HLR:p = .015). In field conditions, we found that males with higher body condition indices express stressed phenotypes more than males with lower body condition indices (p = .002). However, females expressed similar stress loads across all body conditions (p = .900). Testosterone concentrations were assayed in free-living turtles and were not related to any of the immune parameters. Our results suggest that the immune systems play an important role in balancing sex-specific responses to different selective pressures inS. minor.

Deletion of Bmal1 Impairs Pancreatic beta-Cell Function via Mitochondrial Signaling Pathway

BIOMED RESEARCH INTERNATIONAL

Authors: Ye, Lu; Wu, Huaxiang; Xu, Weihong

Several studies have demonstrated that brain and muscle Arnt-like protein-1 (Bmal1) acts as a core clock gene for maintaining normal cell function, including hepatocytes and cardiomyocytes. Loss of Bmal1 is associated with type 2 diabetes due to pancreatic beta-cell failure. However, little information is available about its role and mechanism in pancreatic beta-cell. To address this, we investigated the consequences of Bmal1 inhibition in an insulinoma cell line (INS-1) by using small interfering RNA (siRNA). We observed that knockout of Bmal1 impaired glucose-stimulated insulin secretion in beta-cell. Meanwhile, the depletion of Bmal1 in beta-cell caused an adverse change in mitochondrial membrane potential and mitochondrial architecture. Deletion of Bmal1 attenuated mRNA and protein expression of mitofusin 1 (Mfn1) and mitofusin 2 (Mfn2) and enhanced the expression of fission 1 (Fis1). In summary, the deletion of Bmal1 impaired beta-cell function may be via the mitochondrial signaling pathway in INS-1 cells.

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