[1] Jiang LY. Pathogenesis and therapy progress of periodontal disease[J]. Modern Medicine and Health, 2010, 26(14):2167-2169. (in Chinese)
姜丽艳. 牙周病的病因与治疗进展[J]. 现代医药卫生, 2010, (14): 2167-2169.
[2]Wiebe CB, Silver JG, Larjava HS. Early-onset periodontitis associated with Weary-Kindler syndrome: a case report[J]. J Periodontol, 1996, 67(10): 1004-1010.
[3]Techanukul T, Sethuraman G, Zlotogorski A, et al. Novel and recurrent FERMT1 gene mutations in Kindler syndrome[J]. Acta Derm Venereol, 2011, 91(3): 267-270.
[4]Kloeker S, Major MB, Calderwood DA, et al. The Kindler syndrome protein is regulated by transforming growth factor-beta and involved in integrin-mediated adhesion[J]. J Biol Chem, 2004, 279(8): 6824-6833.
[5]Petricca G, Leppilampi M, Jiang G, et al. Localization and potential function of kindlin-1 in periodontal tissues[J]. Eur J Oral Sci, 2009, 117(5): 518-527.
[6]Kahner BN, Kato H, Banno A, et al. Kindlins, integrin activation and the regulation of talin recruitment to alphaIIbbeta3[J]. PLoS One, 2012, 7(3): e34056.
[7]Larjava H, Plow EF, Wu C. Kindlins: essential regulators of integrin signalling and cell-matrix adhesion[J]. EMBO Rep, 2008, 9(12): 1203-1208.
[8]Herz C, Aumailley M, Schulte C, et al. Kindlin-1 is a phosphoprotein involved in regulation of polarity, proliferation, and motility of epidermal keratinocytes[J]. J Biol Chem, 2006, 281(47): 36082-36090.
[9]Harburger DS, Bouaouina M, Calderwood DA. Kindlin-1 and-2 directly bind the C-terminal region of beta integrin cytoplasmic tails and exert integrin-specific activation effects[J]. J Biol Chem, 2009, 284(17): 11485-11497.
[10]Ussar S, Wang HV, Linder S, et al. The Kindlins: subcellular localization and expression during murine development[J]. Exp Cell Res, 2006, 312(16): 3142-3151.
[11]Wato K, Hara T, Yamana K, et al. An insight into the role of barrier related skin proteins[J]. Int J Pharm, 2012, 427(2): 293-298.
[12]Kern JS, Herz C, Haan E, et al. Chronic colitis due to an epithelial barrier defect: the role of kindlin-1 isoforms[J]. J Pathol, 2007, 213(4): 462-470.
[13]Qu H, Wen T, Pesch M, et al. Partial loss of epithelial phenotype in kindlin-1-deficient keratinocytes[J]. Am J Pathol, 2012, 180(4): 1581-1592.
[14]Heinemann A, He Y, Zimina E, et al. Induction of phenotype modifying cytokines by FERMT1 mutations[J]. Hum Mutat, 2011, 32(4): 397-406.
[15]Pan XD, Chen XCh, Zhu YG, et al. Effect of inflammatory responses in microglia induced by oligomeric β-amyloid 1-42 on neuronal cells[J]. Acta Anatomica Sinica, 2008, 39(6): 804-809. (in Chinese )
潘晓东, 陈晓春, 朱元贵, 等. 寡聚态β-淀粉样肽1~42可通过胶质-炎症反应损伤神经元[J]. 解剖学报, 2008, 39(6): 804-809.
[16]Sin S, Bonin F, Petit V, et al. Role of the focal adhesion protein kindlin-1 in breast cancer growth and lung metastasis[J]. J Natl Cancer Inst, 2011, 103(17): 1323-1337.
[17]Wada M, Masuda K, Tsuruta D, et al. Case of Kindler syndrome resulting from mutation in the FERMT1 gene[J]. J Dermatol, 2012.
[18]Lai-Cheong JE, Moss C, Parsons M, et al. Revertant mosaicism in Kindler syndrome[J]. J Invest Dermatol, 2012, 132(31): 730-732.
[19]Larjava H, Koivisto L, Hakkinen L, et al. Epithelial integrins with special reference to oral epithelia[J]. J Dent Res, 2011, 90(12): 1367-1376. |