مجموعهٔ تمایزی ۹۳ (انگلیسی: Cluster of Differentiation 93) یک پروتئین است که در انسان توسط ژن «CD93» کُدگذاری میشود.[۵][۶][۷]
این مولکول یک پروتئین تراپوستهای سیتایپ است که نه تنها در فرایندهای چسبندگی سلولبهسلول، بلکه در سیستم دفاعی میزبان نقش دارد.[۷]
این پروتئین همچنین نقش مهمی در رشد و تکامل تومورهای گلیوما ایفا میکند. حذف این ژن در موشهای آزمایشگاهی، سبب رشد آهستهتر تومور و بهبود بقای آنها میشود.[۸] در این تومورها همچنین، فیبرسازی فیبرونکتین مختل شده و کیزانِ فعالشدگی اینتگرین بتا ۱ کاهش مییابد.[۹]
↑"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.
↑Nepomuceno RR, Henschen-Edman AH, Burgess WH, Tenner AJ (February 1997). "cDNA cloning and primary structure analysis of C1qR(P), the human C1q/MBL/SPA receptor that mediates enhanced phagocytosis in vitro". Immunity. 6 (2): 119–29. doi:10.1016/S1074-7613(00)80419-7. PMID9047234.
↑Webster SD, Park M, Fonseca MI, Tenner AJ (January 2000). "Structural and functional evidence for microglial expression of C1qR(P), the C1q receptor that enhances phagocytosis". Journal of Leukocyte Biology. 67 (1): 109–16. PMID10648005.
↑Langenkamp E, Zhang L, Lugano R, Huang H, Elhassan TE, Georganaki M, Bazzar W, Lööf J, Trendelenburg G, Essand M, Pontén F, Smits A, Dimberg A (November 2015). "Elevated expression of the C-type lectin CD93 in the glioblastoma vasculature regulates cytoskeletal rearrangements that enhance vessel function and reduce host survival". Cancer Research. 75 (21): 4504–16. doi:10.1158/0008-5472.CAN-14-3636. PMID26363010.
Tenner AJ (August 1998). "C1q receptors: regulating specific functions of phagocytic cells". Immunobiology. 199 (2): 250–64. doi:10.1016/s0171-2985(98)80031-4. PMID9777410.
Ghebrehiwet B, Peerschke EI, Hong Y, Munoz P, Gorevic PD (June 1992). "Short amino acid sequences derived from C1q receptor (C1q-R) show homology with the alpha chains of fibronectin and vitronectin receptors and collagen type IV". Journal of Leukocyte Biology. 51 (6): 546–56. PMID1377218.
Eggleton P, Lieu TS, Zappi EG, Sastry K, Coburn J, Zaner KS, Sontheimer RD, Capra JD, Ghebrehiwet B, Tauber AI (September 1994). "Calreticulin is released from activated neutrophils and binds to C1q and mannan-binding protein". Clinical Immunology and Immunopathology. 72 (3): 405–9. doi:10.1006/clin.1994.1160. PMID8062452.
Stuart GR, Lynch NJ, Day AJ, Schwaeble WJ, Sim RB (December 1997). "The C1q and collectin binding site within C1q receptor (cell surface calreticulin)". Immunopharmacology. 38 (1–2): 73–80. doi:10.1016/S0162-3109(97)00076-3. PMID9476117.
Norsworthy PJ, Taylor PR, Walport MJ, Botto M (August 1999). "Cloning of the mouse homolog of the 126-kDa human C1q/MBL/SP-A receptor, C1qR(p)". Mammalian Genome. 10 (8): 789–93. doi:10.1007/s003359901093. PMID10430665.
Joseph K, Shibayama Y, Ghebrehiwet B, Kaplan AP (January 2001). "Factor XII-dependent contact activation on endothelial cells and binding proteins gC1qR and cytokeratin 1". Thrombosis and Haemostasis. 85 (1): 119–24. PMID11204562.
Steinberger P, Szekeres A, Wille S, Stöckl J, Selenko N, Prager E, Staffler G, Madic O, Stockinger H, Knapp W (January 2002). "Identification of human CD93 as the phagocytic C1q receptor (C1qRp) by expression cloning". Journal of Leukocyte Biology. 71 (1): 133–40. PMID11781389.
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