MOG (35-55)

MOG (35-55) is a 35-55 fragment of myelin oligodendrocyte glycoprotein.

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货号: ajci18628
CAS: 149635-73-4
别名: 髓鞘少突胶质细胞糖蛋白,endrocyte Glycoprotein Peptide (35-55)
分子式: C118H177N35O29S
分子量: 2581.97
纯度: >98%
溶解度: ≥ 32.25mg/mL in Water, ≥ 86 mg/mL in DMSO
储存: Desiccate at -20°C
库存: 现货

Background

MOG (35-55) is a 35-55 fragment of myelin oligodendrocyte glycoprotein ^[1]. Immunizing mice with MOG (35-55) peptide to induce experimental autoimmune encephalomyelitis (EAE), it causes inflammation (macrophages and CD3+ T lymphocytes), demyelination, and axonal loss ^[1]. MOG (35-55) is often used to model EAE in mice for evaluating various drug treatments ^[2].

Axon loss in the medial dorsal column (fasciculus gracilis), which is often damaged in this model of EAE, was detected as early as 7 days post-immunization (p.i.), with a loss of about 11% of axons in the defined counting area. A further 10% loss was observed by day 12 p.i., at which time behavioral disease was just beginning to become apparent ^[1]. T lymphocytes were detected infiltrating the spinal cord as early as day 7 p.i. CD3-immunoreactivity increased 5-fold ^[1]. MOG (35-55) immunized mice developed severe parenchymal infiltration in the spinal cords on day 9, day 13 and day 16, and mice showed heavy infiltration of the cerebral meninges, which prevailed in the region of the hippocampus involving the lateral and the third ventricle ^[3]. MOG (35-55)-induced EAE showed the cerebellar white matter infiltrates in all mice on days 13 and 16 ^[3].

参考文献:
[1]. Jones M V, Nguyen T T, Deboy C A, et al. Behavioral and pathological outcomes in MOG 35-55 experimental autoimmune encephalomyelitis[J]. Journal of neuroimmunology, 2008, 199(1-2): 83-93.
[2]. Steinman L, Zamvil S S. Virtues and pitfalls of EAE for the development of therapies for multiple sclerosis[J]. Trends in immunology, 2005, 26(11): 565-571.
[3]. Kuerten S, Kostova-Bales D A, Frenzel L P, et al. MP4-and MOG: 35-55-induced EAE in C57BL/6 mice differentially targets brain, spinal cord and cerebellum[J]. Journal of neuroimmunology, 2007, 189(1-2): 31-40.

Protocol

Cell experiment [1]:
Cell lines
Preparation Method	To prepare T cell lines specific for MOG (35-55) peptide, C57BL/6 mice were immunized s.c. in the flanks with 0.2 ml of an emulsion containing 200 μg of MOG (35-55) in saline and an equal volume of CFA containing 400 μg Mycobacterium tuberculosis H37RA. Ten days after immunization, lymph node cells were cultured with MOG (35-55) (20 μg/ml) at 8 × 106 cells/ml in stimulation medium (RPMI 1640 medium supplemented with nonessential amino acids, sodium pyruvate, 2-ME, and 10% FBS) for 48 h. The T cells were expanded in medium containing IL-2 (100 U/ml).
Reaction Conditions	20 μg/ml, 5-10 days
Applications	After 5-10 days in culture, the T cell lines responded specifically to MOG (35-55) peptide.
Animal experiment [2]:
Animal models	6-8 weeks old female C57BL/6 mice
Preparation Method	Mice were immunized subcutaneously at the base of the tail with 100 μl of mouse MOG (35-55) peptide emulsified in complete Freund's adjuvant (CFA). Peptide was dissolved in phosphate-buffered saline (PBS) at 2 mg/ml, mixed at a 1:1 ratio with complete adjuvant (8 mg/ml heat-killed Mycobacterium tuberculosis (H37 RA) in incomplete Freund's adjuvant (IFA)), and emulsified by the syringe-extrusion method with two rubber-free Luer-Lock syringes (Air-Tite) connected by a 3-way stopcock until a stable emulsion was formed (approx. 10 min). Each mouse received 100 μg of peptide (and 400 μg of M. tuberculosis). On the day of immunization and two days later, 250 ng of pertussis toxin in 100 μl PBS was administered intravenously.
Dosage form	Subcutaneous injection, 100 μg in 100 μl
Applications	Immunization of C57BL/6 mice with MOG (35-55) caused inflammation and axon loss in the spinal cord but resulted in only minimal demyelination
参考文献: [1]: Ito A, Matejuk A, Hopke C, et al. Transfer of severe experimental autoimmune encephalomyelitis by IL-12-and IL-18-potentiated T cells is estrogen sensitive[J]. The Journal of Immunology, 2003, 170(9): 4802-4809. [2]: Jones M V, Nguyen T T, Deboy C A, et al. Behavioral and pathological outcomes in MOG 35-55 experimental autoimmune encephalomyelitis[J]. Journal of neuroimmunology, 2008, 199(1-2): 83-93.