Nzm2410

Manufactured by Jackson ImmunoResearch

Sourced in United States

NZM2410 is a laboratory equipment product offered by Jackson ImmunoResearch. It serves a core function, but a detailed description while maintaining an unbiased and factual approach is not available.

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Lab products found in correlation

Mrl lpr, by Jackson ImmunoResearch (2 mentions) Nzb nzw f1, by Jackson ImmunoResearch (1 mentions) C57bl 6 b6, by Jackson ImmunoResearch (1 mentions) Mrl mp, by Jackson ImmunoResearch (1 mentions) C57bl 6, by Jackson ImmunoResearch (1 mentions)

Close spelling variants of this product

NZM2410/J NZM2410/J (NZM2410) NZM2410 mice

8 protocols using nzm2410

Ethical Animal Research on Autoimmune Mice

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This study was carried out in accordance with the recommendations of the ethical guidelines for biomedical research on human participants laid down by the Indian Council of Medical Research with written informed consent from all subjects. Patients on follow-up were females (aged between 23 and 45 years) of North Indian ethnicity. All subjects gave written informed consent in accordance with the Declaration of Helsinki. The protocol was approved by the Institutional Human Ethics Committee of the National Institute of Immunology.
This study was carried out in accordance with the recommendations of Committee for the Purpose of Control and Supervision of Experiments on Animals (CPCSEA). The protocol was approved by the Institutional Animal Ethics Committee (IAEC Number: 323/13) of the National Institute of Immunology. NZM2410 (hereafter referred to as NZM), NZB × NZW F1 (hereafter referred to as NZB/W F1), FVB and C57BL/6 mice were obtained from The Jackson Laboratory and maintained at the National Institute of Immunology, New Delhi. Female mice were used for all experiments.

Jain S., Bose A., Bastia B., Sharma H., Sachdeva R., Jain A.K, & Pal R. (2017). Oxidized Hemoglobin Is Antigenic and Immunogenic in Lupus. Frontiers in Immunology, 8, 732.

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Murine Model of Kidney Disease Progression

Cited 1 time

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Female/male C57BL/6 (B6) and NZM2410 mice were obtained from Jackson
Laboratories (Bar Harbor, Maine, USA). Mouse maintenance and protocols were
approved by the Institutional Animal Care and Use Committee at The Ohio State
University Wexner Medical Center (OSUWMC). The animal facility was maintained at
22-23°C and 30-50% relative humidity with a 12-hour light/dark cycle;
chow and water were supplied ad libitum. Blood urea nitrogen (BUN) levels and
weights were measured biweekly. As clinical indicators of kidney damage,
experimental removal criteria was defined by a threshold of 20% weight loss and
a BUN level above 50 mg/dL, as characterized previously (7 (link)). For all mice, disease progression was monitored
and mice were removed when reaching these removal criteria.

Young N.A., Jablonski K., Schwarz E., Okafor I., Hampton J., Valiente G.R., Henry C., Harb P., Barger J., Bratasz A., Kalyanasundaram A., Ardoin S.P, & Jarjour W.N. (2020). Pathological Manifestation of Autoimmune Myocarditis is Detected Prior to Glomerulonephritis in a Murine Model of Lupus Nephritis. Lupus, 29(13), 1790-1799.

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Lupus-prone Murine Models and Blood Analysis

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Female inbred lupus-prone mice (NZM2410 and NZB x NZW (F1), referred to as NZM and B/W F1, respectively) and healthy mice (BALB/c, FVB) were obtained from The Jackson Laboratory. Animals were bred at the Small Animal Facility of the National Institute of Immunology, New Delhi. For some experiments, B/W F1 mice were subjected to ovariectomy at 6 weeks of age. Blood samples were collected from the retro-orbital vein under anesthesia.

De A., Sachdeva R., Bose A., Malik M., Jayachandran N, & Pal R. (2018). Human Chorionic Gonadotropin Influences Systemic Autoimmune Responses. Frontiers in Endocrinology, 9, 742.

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Mouse Strains for Lupus Research

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NZB, NZW, NZM2410, MRL-lpr, MRL/Mp, B6.NZM^Sle1/2/3, C57BL/6, BXSB/Mp, and BXSB.B6-Yaa mice were purchased from Jackson Laboratories (Bar Harbor, ME, USA). All animals were bred at the animal facility of Renji Hospital, School of Medicine, Shanghai Jiao Tong University. The NZB/W F1 strain was generated by breeding male NZW and female NZB mice. We used the commonly used C57BL/6 mice as a reference strain, and all statistical analyses were based on comparisons with C57BL/6 mice in this study unless otherwise indicated.

Zhou Z., Ma J., Xiao C., Han X., Qiu R., Wang Y., Zhou Y., Wu L., Huang X, & Shen N. (2016). Phenotypic and functional alterations of pDCs in lupus-prone mice. Scientific Reports, 6, 20373.

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Murine Lupus Susceptibility Genetics

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C57BL/6 (B6), MRL.lpr and NZM2410 mice were obtained from The Jackson Laboratory and bred in our animal facility. The derivation of B6 congenic mice bearing different NZM2410-derived lupus susceptibility intervals has been detailed previously (51 (link)). B6.Sle1.Sle3 mice, bicongenic two lupus susceptibility intervals Sle1 and Sle3, were previously derived by intercrossing the respective monocongenic strains (4 (link)) . All mice used for this study were bred and housed in a specific-pathogen-free colony at UT Southwestern Medical Center Department of Animal Resources, in Dallas, TX. Both male and female mice were used, and any observed sex differences are noted. Animal experiments were approved by the Institutional Animal Care and Use Committee (IACUC) at UT Southwestern Medical Center at Dallas.

Wu T., Ye Y., Min S.Y., Zhu J., Khobahy E., Zhou J., Yan M., Hemachandran S., Pathak S., Zhou X.J., Andreeff M, & Mohan C. (2014). Targeting multiple signaling axes and oxidative stress using a synthetic triterpenoid prevents murine lupus nephritis. Arthritis & rheumatology (Hoboken, N.J.), 66(11), 3129-3139.

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Generating Sle1.Sle3 VISTA-Deficient Mice

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B6.NZMSle1.Sle2.Sle3, (NZB × NZW)F1, and NZM2410 mice were purchased from The Jackson Laboratory, and female B6 mice were purchased from the National Cancer Institute (Frederick, MD). B6.VISTA^−/− mice were bred as described previously (17 (link)). To generate Sle1.Sle3 VISTA^−/− mice, male and female B6.NZMSle1.Sle2.Sle3 and VISTA^−/− mice were interbred. According to instructions from the laboratory of Dr. Laurence Morel (Department of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville), genotyping was performed to identify Sle1 (D1Mit47, D1Mit15, D1Mit113, and D1Mit155), Sle2 (D4Mit6, D4Mit329, and D4Mit72), and Sle3 (CKMM, D7Mit157, and D7Mit40) loci. The absence of all markers for Sle2 was confirmed by genotyping. This was further confirmed by a loss of the “tan” coat color appearance. Sle1.Sle3 VISTA^−/− mice were all gray. All mice were housed in the pathogen-free facility at the Geisel School of Medicine at Dartmouth.

Ceeraz S., Sergent P.A., Plummer S.F., Schned A.R., Pechenick D., Burns C.M, & Noelle R.J. (2017). VISTA Deficiency Accelerates the Development of Fatal Murine Lupus Nephritis. Arthritis & rheumatology (Hoboken, N.J.), 69(4), 814-825.

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Lupus Murine Models Characterization

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Congenic control (C57BL/6 or B6), Axl^−/−, Mrl-lpr, BXSB, and NZM2410 mice were purchased from the Jackson Laboratory (Bar Harbor, ME) or Taconic Farms (Hudson, NY). B6·Sle1 [23 (link)], B6·Sle3 [24 (link)], B6·Yaa [25 (link)], B6.Lyn^−/− [26 (link)], and BWF1 [27 ] mice were bred in our mouse colony. Mice used for this study were 3 to 8 month old males and females maintained in a stress-free environment. The Animal Care and Use Committee at the University of Texas Southwestern Medical Center approved all experiments using mice.

Orme J.J., Du Y., Vanarsa K., Mayeux J., Li L., Mutwally A., Arriens C., Min S., Hutcheson J., Davis L.S., Chong B.F., Satterthwaite A.B., Wu T, & Mohan C. (2016). Heightened cleavage of Axl receptor tyrosine kinase by ADAM metalloproteases may contribute to disease pathogenesis in SLE. Clinical immunology (Orlando, Fla.), 169, 58-68.

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Inbred Lupus Mice for Research

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Female inbred lupus-prone mice (NZM2410, hereafter referred to as NZM) and healthy mice (FVB/J, hereafter referred to as FVB) were obtained from The Jackson Laboratory. Animals were bred at the Small Animal Facility of the National Institute of Immunology, New Delhi.

Sachdeva R, & Pal R. (2022). A pregnancy hormone-cell death link promotes enhanced lupus-specific immunological effects. Frontiers in Immunology, 13, 1051779.

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