Mouse Anti-Human INS Hybridoma [BF0E7] (CSC-H1269)

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

General Information


Immunogen
Zinc containing crystalline human insulin
Isotype
IgG1, kappa light chain
Fusion Species
Mouse X Mouse Hybridoma
Immunological Donor
Mouse spleen
Myeloma
Sp2/0-Ag14
Clone
BF0E7
Cell Line Description
Animals were immunized with zinc containing crystalline human insulin. Spleen cells were fused with Sp2/0-Ag14 myeloma cells. The antibody binds to residues A8-10 (THR, SER, ILE) of human insulin. The antibody cross-reacts with insulin from pig, rabbit and rat and pro-insulin from cow and pig. 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.
Storage
Liquid nitrogen vapor phase.




Freezing medium: to complete growth medium, add 5%(v/v) DMSO

Target


Synonyms
INS; insulin; proinsulin; ILPR; IRDN; IDDM2; MODY10;
Entrez Gene ID
UniProt ID

Citations


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References


Combined transcriptome and proteome profiling of the pancreatic beta-cell response to palmitate unveils key pathways of beta-cell lipotoxicity

BMC GENOMICS

Authors: Lytrivi, Maria; Ghaddar, Kassem; Lopes, Miguel; Rosengren, Victoria; Piron, Anthony; Yi, Xiaoyan; Johansson, Henrik; Lehtio, Janne; Igoillo-Esteve, Mariana; Cunha, Daniel A.; Marselli, Lorella; Marchetti, Piero; Ortsater, Henrik; Eizirik, Decio L.; Cnop, Miriam

BackgroundProlonged exposure to elevated free fatty acids induces beta -cell failure (lipotoxicity) and contributes to the pathogenesis of type 2 diabetes. In vitro exposure of beta -cells to the saturated free fatty acid palmitate is a valuable model of lipotoxicity, reproducing features of beta -cell failure observed in type 2 diabetes. In order to map the beta -cell response to lipotoxicity, we combined RNA-sequencing of palmitate-treated human islets with iTRAQ proteomics of insulin-secreting INS-1E cells following a time course exposure to palmitate.ResultsCrossing transcriptome and proteome of palmitate-treated beta -cells revealed 85 upregulated and 122 downregulated genes at both transcript and protein level. Pathway analysis identified lipid metabolism, oxidative stress, amino-acid metabolism and cell cycle pathways among the most enriched palmitate-modified pathways. Palmitate induced gene expression changes compatible with increased free fatty acid mitochondrial import and beta -oxidation, decreased lipogenesis and modified cholesterol transport. Palmitate modified genes regulating endoplasmic reticulum (ER) function, ER-to-Golgi transport and ER stress pathways. Furthermore, palmitate modulated cAMP/protein kinase A (PKA) signaling, inhibiting expression of PKA anchoring proteins and downregulating the GLP-1 receptor. SLC7 family amino-acid transporters were upregulated in response to palmitate but this induction did not contribute to beta -cell demise. To unravel critical mediators of lipotoxicity upstream of the palmitate-modified genes, we identified overrepresented transcription factor binding sites and performed network inference analysis. These identified LXR, PPAR alpha, FOXO1 and BACH1 as key transcription factors orchestrating the metabolic and oxidative stress responses to palmitate.ConclusionsThis is the first study to combine transcriptomic and sensitive time course proteomic profiling of palmitate-exposed beta -cells. Our results provide comprehensive insight into gene and protein expression changes, corroborating and expanding beyond previous findings. The identification of critical drivers and pathways of the beta -cell lipotoxic response points to novel therapeutic targets for type 2 diabetes.

Feeding state functionally reconfigures a sensory circuit to drive thermosensory behavioral plasticity

ELIFE

Authors: Takeishi, Asuka; Yeon, Jihye; Harris, Nathan; Yang, Wenxing; Sengupta, Piali

Internal state alters sensory behaviors to optimize survival strategies. The neuronal mechanisms underlying hunger-dependent behavioral plasticity are not fully characterized. Here we show that feeding state alters C. elegans thermotaxis behavior by engaging a modulatory circuit whose activity gates the output of the core thermotaxis network. Feeding state does not alter the activity of the core thermotaxis circuit comprised of AFD thermosensory and AIY interneurons. Instead, prolonged food deprivation potentiates temperature responses in the AWC sensory neurons, which inhibit the postsynaptic AIA interneurons to override and disrupt AFD-driven thermotaxis behavior. Acute inhibition and activation of AWC and AIA, respectively, restores negative thermotaxis in starved animals. We find that state-dependent modulation of AWC-AIA temperature responses requires INS-1 insulin-like peptide signaling from the gut and DAF-16/ FOXO function in AWC. Our results describe a mechanism by which functional reconfiguration of a sensory network via gut-brain signaling drives state-dependent behavioral flexibility.

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