ACD can configure probes for the various manual and automated assays for INSULIN for RNAscope Assay, or for Basescope Assay compatible for your species of interest.
Nature metabolism
2021 Dec 01
Porniece Kumar, M;Cremer, AL;Klemm, P;Steuernagel, L;Sundaram, S;Jais, A;Hausen, AC;Tao, J;Secher, A;Pedersen, TÅ;Schwaninger, M;Wunderlich, FT;Lowell, BB;Backes, H;Brüning, JC;
PMID: 34931084 | DOI: 10.1038/s42255-021-00499-0
Endocrinology.
2018 Jul 27
Doyle ME, Fiori JL, Gonzalez Mariscal I, Liu QR, Goodstein E, Yang H, Shin YK, Santa-Cruz Calvo S, Indig FE, Egan JM.
PMID: 30060183 | DOI: 10.1210/en.2018-00534
We and others have reported that taste cells in taste buds express many peptides in common with cells in the gut and islets of Langerhans in the pancreas. Islets and taste bud cells express the hormones glucagon and ghrelin, the same ATP-sensitive potassium channel (KATP) responsible for depolarizing the insulin secreting beta (β) cell during glucose-induced insulin secretion, as well as the propeptide processing enzymes PC1/3 and PC2. Given the common expression of functionally specific proteins in taste buds and islets, it is surprising that no one has investigated whether insulin is synthesized in taste bud cells until now. Using immunofluorescence, we demonstrate the presence of insulin in mouse, rat and human taste bud cells. We further prove that insulin is synthesized in individual taste buds and not taken up from the parenchyma by: detection of the post-processing insulin molecule C-peptide and green fluorescence protein (GFP) in taste cells of both insulin 1- and insulin 2-GFP mice, and the presence of the mouse insulin transcript by in situ hybridization (ISH). In addition to our cytology data we measured the level of insulin transcript by qRT-PCR in the anterior and posterior lingual epithelium. These analyses show insulin is translated in the circumvallate and foliate papillae in the posterior but only insulin transcript was detected in the anterior fungiform papillae of rodent tongue. Thus, some taste cells are insulin synthesizing cells generated from a continually replenished source of precursor cells in adult mammalian lingual epithelium.
Diabetologia
2022 Apr 27
El Mehdi, M;Takhlidjt, S;Devère, M;Arabo, A;Le Solliec, MA;Maucotel, J;Bénani, A;Nedelec, E;Duparc, C;Lefranc, B;Leprince, J;Anouar, Y;Prévost, G;Chartrel, N;Picot, M;
PMID: 35476025 | DOI: 10.1007/s00125-022-05706-5
Proc Natl Acad Sci U S A.
2017 Jan 23
Okamoto H, Cavino K, Na E, Krumm E, Kim SY, Cheng X, Murphy AJ, Yancopoulos GD, Gromada J.
PMID: 28115707 | DOI: 10.1073/pnas.1621069114
Inactivating mutations in the insulin receptor results in extreme insulin resistance. The resulting hyperglycemia is very difficult to treat, and patients are at risk for early morbidity and mortality from complications of diabetes. We used the insulin receptor antagonist S961 to induce severe insulin resistance, hyperglycemia, and ketonemia in mice. Using this model, we show that glucagon receptor (GCGR) inhibition with a monoclonal antibody normalized blood glucose and β-hydroxybutyrate levels. Insulin receptor antagonism increased pancreatic β-cell mass threefold. Normalization of blood glucose levels with GCGR-blocking antibody unexpectedly doubled β-cell mass relative to that observed with S961 alone and 5.8-fold over control. GCGR antibody blockage expanded α-cell mass 5.7-fold, and S961 had no additional effects. Collectively, these data show that GCGR antibody inhibition represents a potential therapeutic option for treatment of patients with extreme insulin-resistance syndromes.
Nature metabolism
2023 Feb 01
Iker Etchegaray, J;Kelley, S;Penberthy, K;Karvelyte, L;Nagasaka, Y;Gasperino, S;Paul, S;Seshadri, V;Raymond, M;Marco, AR;Pinney, J;Stremska, M;Barron, B;Lucas, C;Wase, N;Fan, Y;Unanue, E;Kundu, B;Burstyn-Cohen, T;Perry, J;Ambati, J;Ravichandran, KS;
PMID: 36732622 | DOI: 10.1038/s42255-022-00728-0
Proc Natl Acad Sci U S A.
2018 Jul 23
Kleiner S, Gomez D, Megra B, Na E, Bhavsar R, Cavino K, Xin Y, Rojas J, Dominguez-Gutierrez G, Zambrowicz B, Carrat G, Chabosseau P, Hu M, Murphy AJ, Yancopoulos GD, Rutter GA, Gromada J.
PMID: 30038024 | DOI: 10.1073/pnas.1721418115
SLC30A8 encodes a zinc transporter that is primarily expressed in the pancreatic islets of Langerhans. In β-cells it transports zinc into insulin-containing secretory granules. Loss-of-function (LOF) mutations in SLC30A8 protect against type 2 diabetes in humans. In this study, we generated a knockin mouse model carrying one of the most common human LOF mutations for SLC30A8, R138X. The R138X mice had normal body weight, glucose tolerance, and pancreatic β-cell mass. Interestingly, in hyperglycemic conditions induced by the insulin receptor antagonist S961, the R138X mice showed a 50% increase in insulin secretion. This effect was not associated with enhanced β-cell proliferation or mass. Our data suggest that the SLC30A8 R138X LOF mutation may exert beneficial effects on glucose metabolism by increasing the capacity of β-cells to secrete insulin under hyperglycemic conditions.
Cell Rep.
2019 May 14
Tencerova M, Frost M, Figeac F, Nielsen TK, Ali D, Lauterlein JL, Andersen TL, Haakonsson AK, Rauch A, Madsen JS, Ejersted C, Højlund K, Kassem M.
PMID: 31091445 | DOI: 10.1016/j.celrep.2019.04.066
Obesity is associated with increased risk for fragility fractures. However, the cellular mechanisms are unknown. Using a translational approach combining RNA sequencing and cellular analyses, we investigated bone marrow stromal stem cells (BM-MSCs) of 54 men divided into lean, overweight, and obese groups on the basis of BMI. Compared with BM-MSCs obtained from lean, obese BM-MSCs exhibited a shift of molecular phenotype toward committed adipocytic progenitors and increased expression of metabolic genes involved in glycolytic and oxidoreductase activity. Interestingly, compared with paired samples of peripheral adipose tissue-derived stromal cells (AT-MSCs), insulin signaling of obese BM-MSCs was enhanced and accompanied by increased abundance of insulin receptor positive (IR+) and leptin receptor positive (LEPR+) cells in BM-MSC cultures. Their hyper-activated metabolic state was accompanied by an accelerated senescence phenotype. Our data provide a plausible explanation for the bone fragility in obesity caused by enhanced insulin signaling leading to accelerated metabolic senescence of BM-MSCs.
J Physiol. 2019 Jan 9.
2019 Jan 09
Shi Z, Cassaglia PA, Pelletier NE, Brooks VL.
PMID: PMID: 30628058 | DOI: DOI:10.1113/JP277517
Molecular metabolism
2022 Jun 09
Zhang, L;Koller, J;Gopalasingam, G;Qi, Y;Herzog, H;
PMID: 35691527 | DOI: 10.1016/j.molmet.2022.101525
Oncotarget
2018 Dec 25
Heckl SM, Pellinghaus M, Krüger S, Bosselmann C, Wilhelm F, Behrens HM, Schreiber S, Röcken C.
PMID: 30680065 | DOI: 10.18632/oncotarget.26490
Abstract
BACKGROUND:
Metabolic reprogramming in cancer encompasses the insulin receptor (IR) as a player of energy homeostasis and proliferation. We aimed to characterize vascular (VIR) and epithelial (EIR) IR expression in CRC and correlate it with clinico-pathological parameters and survival.
METHODS:
1580 primary CRCs were explored by immunohistochemistry for evaluation of VIR and EIR. Subgroup analyses included in situhybridization for IR isoform A (IR-A) and DNA mismatch repair protein immunohistochemistry. Clinico-pathological and survival parameters were studied.
RESULTS:
High VIR was evident in 63.5% of all CRC samples and was associated with T-stage (P = 0.005). EIR was present in 72.2% and was associated with lower T-stages (P = 0.006) and UICC-stages (P < 0.001). EIR negativity was associated with increased metastasis (P =0.028), nodal spread (P < 0.001), lymphatic invasion (P = 0.008) and a decreased tumor-specific (P = 0.011) and overall survival (P = 0.007; 95%-C.I.: 44.5-84.1). EIR negativity in UICC-stage II was associated with a significantly worse tumor-specific (P = 0.045) and overall (P =0.043) survival. IR-A was expressed in CRC vessels and cells.
CONCLUSIONS:
We demonstrate VIR to be frequent in CRC and characterize EIR negativity as an important prognostic risk factor. The association between EIR negativity and worse survival in UICC-stage II should be prospectively evaluated for an application in therapeutic algorithms.
Description | ||
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sense Example: Hs-LAG3-sense | Standard probes for RNA detection are in antisense. Sense probe is reverse complent to the corresponding antisense probe. | |
Intron# Example: Mm-Htt-intron2 | Probe targets the indicated intron in the target gene, commonly used for pre-mRNA detection | |
Pool/Pan Example: Hs-CD3-pool (Hs-CD3D, Hs-CD3E, Hs-CD3G) | A mixture of multiple probe sets targeting multiple genes or transcripts | |
No-XSp Example: Hs-PDGFB-No-XMm | Does not cross detect with the species (Sp) | |
XSp Example: Rn-Pde9a-XMm | designed to cross detect with the species (Sp) | |
O# Example: Mm-Islr-O1 | Alternative design targeting different regions of the same transcript or isoforms | |
CDS Example: Hs-SLC31A-CDS | Probe targets the protein-coding sequence only | |
EnEm | Probe targets exons n and m | |
En-Em | Probe targets region from exon n to exon m | |
Retired Nomenclature | ||
tvn Example: Hs-LEPR-tv1 | Designed to target transcript variant n | |
ORF Example: Hs-ACVRL1-ORF | Probe targets open reading frame | |
UTR Example: Hs-HTT-UTR-C3 | Probe targets the untranslated region (non-protein-coding region) only | |
5UTR Example: Hs-GNRHR-5UTR | Probe targets the 5' untranslated region only | |
3UTR Example: Rn-Npy1r-3UTR | Probe targets the 3' untranslated region only | |
Pan Example: Pool | A mixture of multiple probe sets targeting multiple genes or transcripts |
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