GP(33-41) | Cytiva思拓凡-Whatman滤纸滤膜滤器

GP(33-41);

GP(33-41) 是一种由 9 个氨基酸残基组成的多肽，它是淋巴细胞性脉络丛脑膜炎病毒 GP1 抗原决定基中的最佳序列，能够上调 RMA-S (Db Kb) 细胞表面 H-2D^b 分子，SC₅₀ 值为 344 nM。

GP(33-41) Chemical Structure

CAS No. : 161928-86-5

规格	价格	是否有货
1 mg	￥500	询问价格货期
5 mg	￥1500	询问价格货期
10 mg	￥2400	询问价格货期

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生物活性	GP(33-41), a 9-aa-long peptide, is the optimal sequence of the GP1 epitope of lymphocytic choriomeningitis virus, and can upregulate H-2D^b molecules at the RMA-S (Db Kb) cell surface with a SC₅₀ of 344 nM^[1].
体外研究 (In Vitro)	GP(33-41) sensitizes MC57 and T2-D^b cells to lysis with ED₅₀s of 0.9±0.6 and 2.5±0.7 nM^[1]. The interaction between T cell receptors (TCR) and peptide-major histocompatibility complex (pMHC) antigens can lead to varying degrees of agonism (T cell activation), or antagonism. The P14 TCR recognises the lymphocytic choriomeningitis virus (LCMV)-derived peptide, GP(33-41) (KAVYNFATC), presents in the context of H-2D^[2]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量	226.98
Formula	CH₃TFKNVY
CAS 号	161928-86-5
Sequence	Lys-Ala-Val-Tyr-Asn-Phe-Ala-Thr-Cys
Sequence Shortening	KAVYNFATC
运输条件	Room temperature in continental US; may vary elsewhere.
储存方式	Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献	[1]. Gairin JE, et al. Optimal lymphocytic choriomeningitis virus sequences restricted by H-2Db major histocompatibility complex class I molecules and presented to cytotoxic T lymphocytes. J Virol. 1995 Apr;69(4):2297-305. [2]. Boulter JM, et al. Potent T cell agonism mediated by a very rapid TCR/pMHC interaction. Eur J Immunol. 2007 Mar;37(3):798-806.

Kinase Assay ^[1]	Binding experiments are performed at 37°C with T2-D^b cells, with a Millipore MultiScreen assay system. The H-2D^b LCMV antigen gp276-286 (SGVENPGGYCL) is radioiodinated, and the radiolabeled peptide is purified. Cells (2×10⁵ per well) are incubated in MultiScreen-HV 96-well filtration plates (pore size, 0.45 mm) with ¹²⁵I-gp276-286 (10 nM [final concentration]) for 90 min at 37°C. Cells are washed three times with ice-cold 1% BSA-PBS and by filtration under vacuum. The radioactivity bound to the cells retained on the filter is counted with a gamma counter. Direct binding is measured in the absence (total binding) or the presence (nonspecific binding) of a 1,000-fold excess (10 mM) of unlabeled gp276-286. Specific binding to H-2D^b is defined as the difference between total binding and nonspecific binding. Nontransfected T2 cells are used as a negative control under the same experimental conditions. Competition assays are performed with increasing concentrations (10^-10 to 10^-5 M) of unlabeled peptides competing against a fixed concentration (10^-8 M) of ¹²⁵Igp276-286. The percent inhibition of binding is calculated as 100 × [1-(counts per minute in the presence of competitor – counts per minute of nonspecific binding)/counts per minute of specific binding]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献	[1]. Gairin JE, et al. Optimal lymphocytic choriomeningitis virus sequences restricted by H-2Db major histocompatibility complex class I molecules and presented to cytotoxic T lymphocytes. J Virol. 1995 Apr;69(4):2297-305. [2]. Boulter JM, et al. Potent T cell agonism mediated by a very rapid TCR/pMHC interaction. Eur J Immunol. 2007 Mar;37(3):798-806.

Kinase Assay
^[1]

Binding experiments are performed at 37°C with T2-D^b cells, with a Millipore MultiScreen assay system. The H-2D^b LCMV antigen gp276-286 (SGVENPGGYCL) is radioiodinated, and the radiolabeled peptide is purified. Cells (2×10⁵ per well) are incubated in MultiScreen-HV 96-well filtration plates (pore size, 0.45 mm) with ¹²⁵I-gp276-286 (10 nM [final concentration]) for 90 min at 37°C. Cells are washed three times with ice-cold 1% BSA-PBS and by filtration under vacuum. The radioactivity bound to the cells retained on the filter is counted with a gamma counter. Direct binding is measured in the absence (total binding) or the presence (nonspecific binding) of a 1,000-fold excess (10 mM) of unlabeled gp276-286. Specific binding to H-2D^b is defined as the difference between total binding and nonspecific binding. Nontransfected T2 cells are used as a negative control under the same experimental conditions. Competition assays are performed with increasing concentrations (10^-10 to 10^-5 M) of unlabeled peptides competing against a fixed concentration (10^-8 M) of ¹²⁵Igp276-286. The percent inhibition of binding is calculated as 100 × [1-(counts per minute in the presence of competitor – counts per minute of nonspecific binding)/counts per minute of specific binding].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

参考文献

[1]. Gairin JE, et al. Optimal lymphocytic choriomeningitis virus sequences restricted by H-2Db major histocompatibility complex class I molecules and presented to cytotoxic T lymphocytes. J Virol. 1995 Apr;69(4):2297-305.

[2]. Boulter JM, et al. Potent T cell agonism mediated by a very rapid TCR/pMHC interaction. Eur J Immunol. 2007 Mar;37(3):798-806.