گلیپیکان ۳

GPC3
معین‌کننده‌ها
نام‌های دیگر	GPC3, DGSX, GTR2-2, MXR7, OCI-5, SDYS, SGB, SGBS, SGBS1, Glypican 3
شناسه‌های بیرونی	OMIM: 300037 MGI: 104903 HomoloGene: 20944 GeneCards: GPC3
موقعیت ژن (انسان)
کروموزوم	کروموزوم X (انسان)
پایان	133,987,100 bp
موقعیت ژن (موش)
کروموزوم	کروموزوم X (موش)
پایان	51,702,827 bp
الگوی گسترش RNA
	More reference expression data
هستی‌شناسی ژن
عملکرد ملکولی	• peptidase inhibitor activity; • GO:0001948، GO:0016582 پیوند پروتئینی; • peptidyl-dipeptidase inhibitor activity; • heparan sulfate proteoglycan binding;
ترکیبات سلولی	• membrane; • anchored component of plasma membrane; • پوسته یاخته; • integral component of plasma membrane; • extracellular region; • lysosomal lumen; • Golgi lumen; • anchored component of membrane; • کافنده‌تن; • extracellular space; • endoplasmic reticulum lumen; • intrinsic component of plasma membrane; • collagen-containing extracellular matrix;
فرایند زیستی	• body morphogenesis; • positive regulation of glucose import; • bone mineralization; • negative regulation of peptidase activity; • negative regulation of growth; • negative regulation of smoothened signaling pathway; • GO:1903364 positive regulation of protein catabolic process; • positive regulation of smoothened signaling pathway; • cell proliferation involved in metanephros development; • lung development; • kidney development; • osteoclast differentiation; • anatomical structure morphogenesis; • mesenchymal cell proliferation involved in ureteric bud development; • mesonephric duct morphogenesis; • coronary vasculature development; • retinoid metabolic process; • cell proliferation involved in kidney development; • positive regulation of endocytosis; • branching involved in ureteric bud morphogenesis; • glycosaminoglycan catabolic process; • glycosaminoglycan biosynthetic process; • negative regulation of epithelial cell proliferation; • positive regulation of BMP signaling pathway; • animal organ morphogenesis; • regulation of growth; • positive regulation of Wnt signaling pathway, planar cell polarity pathway; • anterior/posterior axis specification; • negative regulation of canonical Wnt signaling pathway; • negative regulation of cell population proliferation; • embryonic hindlimb morphogenesis; • پیرایش پسارونویسی; • regulation of signal transduction; • response to bacterium;
	منابع: آمیگو / کوئیک‌گو
هم‌ساخت‌شناسی
	2719
	14734
	ENSG00000147257
	ENSMUSG00000055653
	P51654
	Q8CFZ4
	NM_001164617، NM_001164618، NM_001164619، XM_017029413 NM_004484، NM_001164617، NM_001164618، NM_001164619، XM_017029413
	NM_016697
	NP_001158090، NP_001158091، NP_004475، XP_016884902 NP_001158089، NP_001158090، NP_001158091، NP_004475، XP_016884902; NP_004475.1
	NP_057906
	ویکی‌داده
مشاهده/ویرایش انسان	مشاهده/ویرایش موش

گلیپیکان ۳ (انگلیسی: Glypican 3) یک پروتئین است که در انسان توسط ژن «GPC3» کُدگذاری می‌شود.^[۵]^[۶]^[۷]^[۸] این ژن بر روی بازوی بلندِ کروموزوم ایکس قرار دارد و یک پروتئین ۷۰ کیلو دالتونی را با ۵۸۰ اسید آمینه می‌سازد.^[۹]

اهمیت بالینی

جهش در ژن «GPC3» با بروز «سندرم سیمپسون–گلابی–بیمل نوع ۱» در ارتباط است.^[۱۰]

از این پروتئین می‌توان در تمایز انواع سرطان‌های کبد با تغییرات دیسپلاستیک سیروز استفاده کرد.^[۱۱]

گلیپیکان ۳ یک هدف درمانی امیدبخش برای درمان سرطان کبد و برخی سرطان‌های دیگر است.^[۹]^[۱۲]

منابع

↑ ^۱٫۰ ^۱٫۱ ^۱٫۲ GRCh38: Ensembl release 89: ENSG00000147257 - Ensembl, May 2017
↑ ^۲٫۰ ^۲٫۱ ^۲٫۲ GRCm38: Ensembl release 89: ENSMUSG00000055653 - Ensembl, May 2017
↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
↑ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
↑ Pilia G, Hughes-Benzie RM, MacKenzie A, Baybayan P, Chen EY, Huber R, Neri G, Cao A, Forabosco A, Schlessinger D (March 1996). "Mutations in GPC3, a glypican gene, cause the Simpson-Golabi-Behmel overgrowth syndrome". Nature Genetics. 12 (3): 241–7. doi:10.1038/ng0396-241. PMID 8589713.
↑ Veugelers M, Vermeesch J, Watanabe K, Yamaguchi Y, Marynen P, David G (October 1998). "GPC4, the gene for human K-glypican, flanks GPC3 on xq26: deletion of the GPC3-GPC4 gene cluster in one family with Simpson-Golabi-Behmel syndrome". Genomics. 53 (1): 1–11. doi:10.1006/geno.1998.5465. PMID 9787072.
↑ "Entrez Gene: GPC3 glypican 3".
↑ Jakubovic BD, Jothy S (April 2007). "Glypican-3: from the mutations of Simpson-Golabi-Behmel genetic syndrome to a tumor marker for hepatocellular carcinoma". Experimental and Molecular Pathology. 82 (2): 184–9. doi:10.1016/j.yexmp.2006.10.010. PMID 17258707.
↑ ^۹٫۰ ^۹٫۱ Ho M, Kim H (February 2011). "Glypican-3: a new target for cancer immunotherapy". European Journal of Cancer. 47 (3): 333–8. doi:10.1016/j.ejca.2010.10.024. PMC 3031711. PMID 21112773.
↑ Davoodi J, Kelly J, Gendron NH, MacKenzie AE (June 2007). "The Simpson-Golabi-Behmel syndrome causative glypican-3, binds to and inhibits the dipeptidyl peptidase activity of CD26". Proteomics. 7 (13): 2300–10. doi:10.1002/pmic.200600654. PMID 17549790.
↑ Anatelli F, Chuang ST, Yang XJ, Wang HL (August 2008). "Value of glypican 3 immunostaining in the diagnosis of hepatocellular carcinoma on needle biopsy". American Journal of Clinical Pathology. 130 (2): 219–23. doi:10.1309/WMB5PX57Y4P8QCTY. PMID 18628090.
↑ Li N, Gao W, Zhang YF, Ho M (November 2018). "Glypicans as Cancer Therapeutic Targets". Trends in Cancer. 4 (11): 741–754. doi:10.1016/j.trecan.2018.09.004. PMC 6209326. PMID 30352677.

مشارکت‌کنندگان ویکی‌پدیا. «Glypican 3». در دانشنامهٔ ویکی‌پدیای انگلیسی، بازبینی‌شده در ۱۴ سپتامبر ۲۰۱۹.

برای مطالعهٔ بیشتر

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این یک مقالهٔ خرد زیست‌شناسی مولکولی است. می‌توانید با گسترش آن به ویکی‌پدیا کمک کنید.

[refGRCh38Ensembl-1] ۱٫۰ ^۱٫۱ ^۱٫۲ GRCh38: Ensembl release 89: ENSG00000147257 - Ensembl, May 2017

[refGRCm38Ensembl-2] ۲٫۰ ^۲٫۱ ^۲٫۲ GRCm38: Ensembl release 89: ENSMUSG00000055653 - Ensembl, May 2017

[3] "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[4] "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[pmid8589713-5] Pilia G, Hughes-Benzie RM, MacKenzie A, Baybayan P, Chen EY, Huber R, Neri G, Cao A, Forabosco A, Schlessinger D (March 1996). "Mutations in GPC3, a glypican gene, cause the Simpson-Golabi-Behmel overgrowth syndrome". Nature Genetics. 12 (3): 241–7. doi:10.1038/ng0396-241. PMID 8589713.

[pmid9787072-6] Veugelers M, Vermeesch J, Watanabe K, Yamaguchi Y, Marynen P, David G (October 1998). "GPC4, the gene for human K-glypican, flanks GPC3 on xq26: deletion of the GPC3-GPC4 gene cluster in one family with Simpson-Golabi-Behmel syndrome". Genomics. 53 (1): 1–11. doi:10.1006/geno.1998.5465. PMID 9787072.

[entrez_2719-7] "Entrez Gene: GPC3 glypican 3".

[pmid17258707-8] Jakubovic BD, Jothy S (April 2007). "Glypican-3: from the mutations of Simpson-Golabi-Behmel genetic syndrome to a tumor marker for hepatocellular carcinoma". Experimental and Molecular Pathology. 82 (2): 184–9. doi:10.1016/j.yexmp.2006.10.010. PMID 17258707.

[Ho_2011-9] ۹٫۰ ^۹٫۱ Ho M, Kim H (February 2011). "Glypican-3: a new target for cancer immunotherapy". European Journal of Cancer. 47 (3): 333–8. doi:10.1016/j.ejca.2010.10.024. PMC 3031711. PMID 21112773.

[pmid17549790-10] Davoodi J, Kelly J, Gendron NH, MacKenzie AE (June 2007). "The Simpson-Golabi-Behmel syndrome causative glypican-3, binds to and inhibits the dipeptidyl peptidase activity of CD26". Proteomics. 7 (13): 2300–10. doi:10.1002/pmic.200600654. PMID 17549790.

[11] Anatelli F, Chuang ST, Yang XJ, Wang HL (August 2008). "Value of glypican 3 immunostaining in the diagnosis of hepatocellular carcinoma on needle biopsy". American Journal of Clinical Pathology. 130 (2): 219–23. doi:10.1309/WMB5PX57Y4P8QCTY. PMID 18628090.

[Gao_W_2018-12] Li N, Gao W, Zhang YF, Ho M (November 2018). "Glypicans as Cancer Therapeutic Targets". Trends in Cancer. 4 (11): 741–754. doi:10.1016/j.trecan.2018.09.004. PMC 6209326. PMID 30352677.

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