Heparanase: busy at the cell surface.
Heparanase: busy at the cell surface.
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DOI：
10.1016/j.tibs.2009.06.005
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发表时间：
2009-10
影响因子：
13.8
通讯作者：
Vlodavsky, Israel
中科院分区：
文献类型：
--
作者：
Fux, Liat;Ilan, Neta;Sanderson, Ralph D.;Vlodavsky, Israel
乙酰肝素酶活性与肿瘤和内皮细胞下方的细胞外基质的结构重塑密切相关，从而导致细胞侵袭。此外，乙酰肝素酶增强信号级联，导致选定蛋白激酶的磷酸化增强，并增加与侵袭性肿瘤进展相关的基因转录。该功能显然独立于硫酸乙酰肝素和酶活性，并且由位于乙酰肝素酶 C 末端（C 结构域）的新型蛋白质结构域介导。此外，乙酰肝素酶的功能库通过其对多聚糖聚集、脱落和有丝分裂原结合的调节而得到扩展。最近，抑制乙酰肝素酶活性的改良乙二醇裂解肝素被证明可以深刻抑制骨髓瘤和癌细胞产生的肿瘤异种移植物的进展，从而使抗乙酰肝素酶治疗更接近现实。
Heparanase activity is strongly implicated in structural remodeling of the extracellular matrix underlying tumor and endothelial cells that leads to cellular invasion. In addition, heparanase augments signaling cascades leading to enhanced phosphorylation of selected protein kinases and increased gene transcription associated with aggressive tumor progression. This function is apparently independent of heparan sulfate and enzyme activity and is mediated by a novel protein domain localized at the heparanase C-terminus (C-domain). Moreover, the functional repertoire of heparanase is expanded by its regulation of syndecan clustering, shedding, and mitogen binding. Recently, modified glycol-split heparin that inhibits heparanase activity was demonstrated to profoundly inhibit the progression of tumor xenografts produced by myeloma and carcinoma cells thus moving anti-heparanase therapy closer to reality.
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影响因子：
4.8
作者：
Dai, YM;Yang, Y;Sanderson, RD
通讯作者：
Sanderson, RD
影响因子：
4.8
作者：
Gingis-Velitski, S;Zetser, A;Ilan, N
通讯作者：
Ilan, N
影响因子：
4.8
作者：
Goldschmidt, O;Zcharia, E;Vlodavsky, I
通讯作者：
Vlodavsky, I
影响因子：
--
作者：
Casu B;Vlodavsky I;Sanderson RD
通讯作者：
Sanderson RD
影响因子：
3.7
作者：
Chen, Ligong;Sanderson, Ralph D.
通讯作者：
Sanderson, Ralph D.