Idtr mice

Manufactured by Jackson ImmunoResearch

IDTR mice are genetically engineered mice that express an inducible diphtheria toxin receptor (IDTR) gene. This gene allows for the targeted depletion of specific cell populations upon administration of diphtheria toxin.

Automatically generated - may contain errors

Lab products found in correlation

Rosa26tdtomato, by Jackson ImmunoResearch (1 mentions) Gli1 creert2, by Jackson ImmunoResearch (1 mentions) C57bl 6, by Japan SLC (1 mentions) Vav cre, by Jackson ImmunoResearch (1 mentions) Mx1 cre, by Jackson ImmunoResearch (1 mentions) Sodium pentobarbital solution, by Merck Group (1 mentions) Lyve1 cre mice, by Jackson ImmunoResearch (1 mentions) Gfp mice, by Jackson ImmunoResearch (1 mentions) Lyve 1 cre, by Merck Group (1 mentions) Hank s balanced salt solution, by Merck Group (1 mentions)

4 protocols using idtr mice

Lineage Tracing and Cell Ablation

Check if the same lab product or an alternative is used in the 5 most similar protocols

All mouse experiments were performed according to the animal experimental guidelines issued by the Animal Care and Use Committee at Harvard University. Gli1-nLacZ (JAX #008211) Gli1CreER^t2 (JAX #007913), Rosa26tdTomato (JAX #007909) iDTR mice (JAX # 007900), Ptprc^a-Pepc^b mice (JAX #002014) were purchased from Jackson Laboratories (Bar Harbor, ME). For lineage tracing studies 6–7 week old mice received 3 × 0.1mg/kg bodyweight tamoxifen in corn oil / 3% ethanol (Sigma) via intraperitoneal injection 10days before surgery or disease induction unless otherwise stated. All models of organ injury and cell-specific ablation experiments are described in the Supplementary Experimental Procedures.

Kramann R., Schneider R.K., DiRocco D.P., Machado F., Fleig S., Bondzie P.A., Henderson J.M., Ebert B.L, & Humphreys B.D. (2014). Perivascular Gli1+ progenitors are key contributors to injury-induced organ fibrosis. Cell stem cell, 16(1), 51-66.

+ Open protocol

+ Expand

Murine Ischemic Stroke Model

Check if the same lab product or an alternative is used in the 5 most similar protocols

All efforts were made to minimize animal suffering and to reduce the number of animals used. Animals were housed under a 12/12-h light/dark cycle and fed ad libitum. Male 8-wk-old wild-type mice (C57BL/6, obtained from Japan SLC), male Nestin–Cre^ERT2::Stop–EGFP (a generous gift from Dr. I. Imayoshi), male iDTR mice (purchased from the Jackson Laboratory), and male and female Hexb–Cre^ERT2::Stop–YFP mice (50 (link)) were used for a mouse model of ischemic stroke. All experiments were carried out according to the animal experimentation guidelines of Kyushu University, Tokai University, or University of Tokyo, which comply with the NIH Guide for the Care and Use of Laboratory Animals.

Irie T., Matsuda T., Hayashi Y., Matsuda-Ito K., Kamiya A., Masuda T., Prinz M., Isobe N., Kira J.I, & Nakashima K. (2023). Direct neuronal conversion of microglia/macrophages reinstates neurological function after stroke. Proceedings of the National Academy of Sciences of the United States of America, 120(42), e2307972120.

+ Open protocol

+ Expand

Jak2V617F Knock-in Mouse Model

Check if the same lab product or an alternative is used in the 5 most similar protocols

All mice used in this study were on the C57BL/6 background. Floxed heterozygous Jak^V617F/+ knock-in animals (a gift of Dr. Ann Mullally (13 (link))) were bred with Pf4-Cre transgenic mice (a gift of Dr. Radek Skoda(23 (link))) to induce Jak2^V617F expression in megakaryocyte lineage-committed cells. Vav-Cre (Stock# 008610) and Mx1-Cre (Stock# 003556) transgenic mice were purchased from Jackson Laboratory (Bar Harbor, ME) and bred with Jak2^V617F/+ mice to induce pan-hematopoietic Jak2^V617F expression. For megakaryocyte depletion studies, iDTR mice (which harbor a conditional Cre-inducible diphtheria toxin receptor (DTR) (24 (link))) were obtained from Jackson Laboratory (Stock# 007900) and crossed to Pf4-Cre⁺ mice. For lineage tracing studies, mTmG Cre switch reporter mice (25 (link)) were obtained from Jackson Laboratory (Stock# 007676) and bred to Jak2^V617F/+; Pf4-Cre⁺ mice to confirm lineage-specific Cre expression. Animal studies were approved by the IACUC of both Northwestern University and Memorial Sloan Kettering Cancer Center.

Woods B., Chen W., Chiu S., Marinaccio C., Fu C., Gu L., Bulic M., Yang Q., Zouak A., Jia S., Suraneni P.K., Xu K., Levine R.L., Crispino J.D, & Wen Q.J. (2019). Activation of JAK/STAT signaling in megakaryocytes sustains myeloproliferation in vivo. Clinical cancer research : an official journal of the American Association for Cancer Research, 25(19), 5901-5912.

+ Open protocol

+ Expand

Targeted Ablation of Lymphatic Vessels

Check if the same lab product or an alternative is used in the 5 most similar protocols

LYVE-1-Cre mice, iDTR mice, and GFP mice were purchased from The Jackson Laboratory. C57BL/6 mice (age, 8 to 10 weeks; weight, ~22 to 25 g) were purchased from Hua Fukang (Beijing, China). The LYVE1-Cre mouse was chosen for its selective enhanced GFP expression in the nuclei of cells expressing LYVE-1. To ablate LYVE1-expressing LVs in a DT-dependent manner, LYVE-1-Cre mice were crossed with iDTR mice (LYVE-1-Cre/iDTR mice). LVs were ablated by administering DT (1.25 ng/g body weight, dissolved in Hanks’ balanced salt solution; Sigma-Aldrich) to LYVE-1-Cre/iDTR mice intravenously unless otherwise indicated. All mice were provided with a standard diet and access to water. Mice were anesthetized and euthanized with 1% sodium pentobarbital solution (0.009 ml/g, Sigma, USA) by intraperitoneal injection. Animals were bred and maintained at Tongji Medical College of Huazhong University of Science and Technology.

Pei G., Yao Y., Yang Q., Wang M., Wang Y., Wu J., Wang P., Li Y., Zhu F., Yang J., Zhang Y., Yang W., Deng X., Zhao Z., Zhu H., Ge S., Han M., Zeng R, & Xu G. (2019). Lymphangiogenesis in kidney and lymph node mediates renal inflammation and fibrosis. Science Advances, 5(6), eaaw5075.

+ Open protocol

+ Expand

About PubCompare

Our mission is to provide scientists with the largest repository of trustworthy protocols and intelligent analytical tools, thereby offering them extensive information to design robust protocols aimed at minimizing the risk of failures.

We believe that the most crucial aspect is to grant scientists access to a wide range of reliable sources and new useful tools that surpass human capabilities.

However, we trust in allowing scientists to determine how to construct their own protocols based on this information, as they are the experts in their field.

Ready to get started?

Revolutionizing how scientists
search and build protocols!