CTLA-4

細胞毒性T淋巴細胞相關抗原4
已知的結構
PDB	直系同源搜索: PDBe RCSB
PDBID列表
	3OSK、1AH1、1H6E、1I85、1I8L、2X44、3BX7
識別號
别名	CTLA4；, ALPS5, CD, CD152, CELIAC3, CTLA-4, GRD4, GSE, IDDM12, cytotoxic T-lymphocyte associated protein 4
外部ID	OMIM：123890 MGI：88556 HomoloGene：3820 GeneCards：CTLA4
相關疾病
	類風濕性關節炎、甲狀腺機能低下症、1型糖尿病、type 1 diabetes mellitus 12、autoimmune lymphoproliferative syndrome due to CTLA4 haploinsuffiency[1]
為以下藥物的標靶
	伊匹單抗[2]
基因位置（人类）
染色体	2號染色體[3]
终止	203,873,965 bp[3]
基因位置（小鼠）
染色体	小鼠1号染色体[4]
终止	60,954,991 bp[4]
RNA表达模式
	查阅更多表达数据
基因本體
分子功能	• 血浆蛋白结合;
細胞組分	• 细胞质的核周区域; • integral component of membrane; • clathrin-coated endocytic vesicle; • 细胞膜; • 高尔基体; • 膜; • external side of plasma membrane; • protein complex involved in cell adhesion; • integral component of plasma membrane;
生物學過程	• B cell receptor signaling pathway; • T cell costimulation; • negative regulation of B cell proliferation; • adaptive immune response; • negative regulation of regulatory T cell differentiation; • 免疫反应; • cellular response to DNA damage stimulus; • immune system process; • positive regulation of apoptotic process; • negative regulation of immune response; • negative regulation of T cell proliferation; • regulation of regulatory T cell differentiation; • regulation of T cell proliferation; • T cell receptor signaling pathway;
	Sources:Amigo / QuickGO
直系同源
	1493
	12477
	ENSG00000163599
	ENSMUSG00000026011
	P16410
	P09793
	NM_001037631; NM_005214
	NM_001281976; NM_009843
	NP_001032720; NP_005205
	NP_001268905; NP_033973
	維基數據

CTLA4又稱CTLA-4（細胞毒性T淋巴細胞相關抗原4，cytotoxic T-lymphocyte-associated protein 4）或CD152（分化群152），是一种蛋白质受体[7]。CTLA-4蛋白由小鼠的Ctla4[8]和人类的CTLA4基因编码[9]。CTLA-4于1991年首次被發現[10]。

参考文献

.
.
GRCh38: Ensembl release 89: ENSG00000163599 - Ensembl, May 2017
GRCm38: Ensembl release 89: ENSMUSG00000026011 - Ensembl, May 2017
. National Center for Biotechnology Information, U.S. National Library of Medicine.
. National Center for Biotechnology Information, U.S. National Library of Medicine.
. The Lancet. Oncology. December 2017, 18 (12): e731–e741. PMID 29208439. doi:10.1016/s1470-2045(17)30607-1.
. Nature. 1987, 328 (6127): 267–70. Bibcode:1987Natur.328..267B. PMID 3496540. doi:10.1038/328267a0.
. European Journal of Immunology. December 1988, 18 (12): 1901–5. PMID 3220103. doi:10.1002/eji.1830181206.
. Science. November 1995, 270 (5238): 985–8. Bibcode:1995Sci...270..985W. JSTOR 2888113. PMID 7481803. doi:10.1126/science.270.5238.985.

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[1] .

[2] .

[refGRCh38Ensembl-3] GRCh38: Ensembl release 89: ENSG00000163599 - Ensembl, May 2017

[refGRCm38Ensembl-4] GRCm38: Ensembl release 89: ENSMUSG00000026011 - Ensembl, May 2017

[5] . National Center for Biotechnology Information, U.S. National Library of Medicine.

[6] . National Center for Biotechnology Information, U.S. National Library of Medicine.

[:0-7] . The Lancet. Oncology. December 2017, 18 (12): e731–e741. PMID 29208439. doi:10.1016/s1470-2045(17)30607-1.

[pmid3496540-8] . Nature. 1987, 328 (6127): 267–70. Bibcode:1987Natur.328..267B. PMID 3496540. doi:10.1038/328267a0.

[pmid3220103-9] . European Journal of Immunology. December 1988, 18 (12): 1901–5. PMID 3220103. doi:10.1002/eji.1830181206.

[Waterhouse_1995-10] . Science. November 1995, 270 (5238): 985–8. Bibcode:1995Sci...270..985W. JSTOR 2888113. PMID 7481803. doi:10.1126/science.270.5238.985.