Nod prkdcscidil2rgem1 smoc mice

Manufactured by Shanghai Model Organisms

The NOD‐PrkdcscidIl2rgem1/Smoc mouse is a laboratory mouse model that is immunodeficient, lacking both functional T and B cells. This model is useful for studying human diseases and evaluating various therapeutic interventions.

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Lab products found in correlation

0.4 μm pore polyester membrane, by Corning (1 mentions) Pneumacult ali medium, by STEMCELL (1 mentions) Growth factor reduced matrigel, by Corning (1 mentions) Indigo, by Berthold Technologies (1 mentions) Nightowl lb 983, by Berthold Technologies (1 mentions)

Close spelling variants of this product

M-NSG (NOD-PrkdcscidIl2rgem1/Smoc) mice

3 protocols using nod prkdcscidil2rgem1 smoc mice

Xenograft Model for Pancreatic Cancer

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Six‐week‐old female NOD‐PrkdcscidIl2rgem1/Smoc mice were purchased from the Shanghai Model Organisms Center, Inc. Samples from patients with PC were cut into small pieces (approximate diameter: 3 mm) and subcutaneously implanted into the axilla of mice. When the tumor volume reached 150 mm³, the mice were administered vehicle or 3 mg/kg AZD5582 by i.v. once a week for 3 weeks, and the tumors and body weights were monitored and measured every 3 days for 3 weeks until euthanasia.
¹⁵ (link) The ethical point was defined as tumor size of approximately 1500 mm³.

Ma Z., Gu Q., Dai Y., Wang Q., Shi W, & Jiao Z. (2023). Therapeutic potential of SHCBP1 inhibitor AZD5582 in pancreatic cancer treatment. Cancer Science, 115(3), 820-835.

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In vitro and in vivo Epithelial Cell Differentiation

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For in vitro differentiation, microbeads-purified epithelial cells were harvested from cultures and plated on inserts of 6.5 mm transwell with 0.4 μm pore polyester membrane (Corning) at a density of 6 × 10⁵ cells/cm², followed by 2–3 days expansion in growth medium then maintained as air–liquid interface in PneumaCult-ALI medium (StemCell Technologies) for 20 days until structures mature. Differentiated cells were fixed for IF staining and meanwhile, preserved in TRIzol for standard RNA isolation.
For in vivo differentiation, cultured cells (3 × 10⁶ cells/injection) were resuspended in Dulbecco’s Modified Eagle’s Medium and pre-mixed 1:1 (v/v) with growth factor reduced Matrigel (Corning) prior to subcutaneous injection on immunodeficient NOD-Prkdc^scidIl2rg^em1/Smoc mice (Shanghai Model Organisms). The 6–8-week-old male and female animals were used for all experiments. Mice were sacrificed at Week 4 post cell injection, and nodule growths were collected for paraffin embedding, sectioning and subsequently IHC/IF assessment. Meanwhile, differentiated structures were preserved in TRIzol for standard RNA isolation. All procedures were conducted under IACUC guidelines and approved protocol by the IACUC committee of Shanghai Sixth People’s Hospital.

Hong Y., Shan S., Gu Y., Huang H., Zhang Q., Han Y., Dong Y., Liu Z., Huang M, & Ren T. (2022). Malfunction of airway basal stem cells plays a crucial role in pathophysiology of tracheobronchopathia osteoplastica. Nature Communications, 13, 1309.

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Generation of Luc-Env+/PD-L1+ NSG Mouse Model

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Female NSG (NOD-Prkdc^scidIl2rg^em1/Smoc) mice aged 4–6 weeks, purchased from Shanghai Model Organisms, were maintained under specific pathogen-free (SPF) conditions. To generate the Luc-Env⁺/PD-L1⁺ mouse model, LEL6 cells were resuspended in PBS at 2 × 10⁶ cells/mL and each NSG mouse was injected intravenously (i.v.) with 2 × 10⁵ LEL6 cells on day 0. The mice were randomly divided into four groups (n = 4). Four days later, 2 × 10⁶ UTD or CAR-T cells were injected into NSG mice via the tail vein. The second-round injections of 2 × 10⁶ UTD or CAR-T cells were performed at Day 11 post LEL6 cell injection. The mice were subjected to weekly bioluminescence imaging using NightOWL LB983 (Berthold, Stuttgart, Germany), and the data were analysed and exported using IndiGO (Berthold).

Pan H., Yang X., Wang J., Liang H., Jiang Z., Zhao L., Wang Y., Liang Z., Shen X., Lin Q., Liang Y., Yang J., Lu P., Zhu Y., Li M., Wang P., Xu J., Lu H, & Zhu H. (2023). Allogeneic gene-edited HIV-specific CAR-T cells secreting PD-1 blocking scFv enhance specific cytotoxic activity against HIV Env+ cells invivo. Virologica Sinica, 38(2), 285-295.

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