Last update 01 Nov 2024

HS x β-galactosidase

Last update 01 Nov 2024

Basic Info

Related Targets

HSβ-galactosidase

Drugs associated with HS x β-galactosidase

AX-552

Target

HS x β-galactosidase

Mechanism

Heparan sulfate sulfatase replacements [+1]

Active Org.

Allievex Corp. [+1]

Originator Org.

Allievex Corp.

Active Indication

Gangliosidosis, GM1

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with HS x β-galactosidase

100 Translational Medicine associated with HS x β-galactosidase

0 Patents (Medical) associated with HS x β-galactosidase

Literatures (Medical) associated with HS x β-galactosidase

01 Sep 2013·Journal of Cellular BiochemistryQ3 · BIOLOGY

The matricellular protein CCN1 suppresses lung cancer cell growth by inducing senescence via the p53/p21 pathway

Q3 · BIOLOGY

Article

Author: Sung, Jung‐Sung ; Wang, Tse‐Yen ; Wang, Jeng‐Jung ; Jim Leu, Shr‐Jeng ; Cheng, Jian‐Yu ; Chen, Chih‐Wei ; Chen, Mei‐Yu

AbstractCCN1, a secreted matrix‐associated molecule, is involved in multiple cellular processes. Previous studies have indicated that expression of CCN1 correlates inversely with the aggressiveness of non‐small‐cell lung carcinoma (NSCLC); however, the underlying mechanisms remain elusive. Using three NSCLC cell line systems, here we show that long‐term treatment of cells with the recombinant CCN1 protein led to a permanent cell cycle arrest in G1 phase; cells remained viable as judged by apoptotic assays. CCN1‐treated NSCLC cells acquired a phenotype characteristic of senescent cells, including an enlarged and flattened cell shape and expression of the senescence‐associated β‐galactosidase. Immunoblot analysis showed that addition of CCN1 increased the abundance of hypo‐phosphorylated Rb, as well as accumulation of p53 and p21. Silencing the expression of p53 or p21 by lentivirus‐mediated shRNA production in cells blocked the CCN1‐induced senescence. Furthermore, a CCN1 mutant defective for binding integrin α6β1 and co‐receptor heparan sulfate proteoglycans was incapable of senescence induction. Our finding that direct addition of CCN1 induces senescence in NSCLC cells provides a potential novel strategy for therapeutic intervention of lung cancers. J. Cell. Biochem. 114: 2082–2093, 2013. © 2013 Wiley Periodicals, Inc.

01 Jun 2010·Journal of Biological ChemistryQ2 · BIOLOGY

Characterization of the Cell-penetrating Properties of the Epstein-Barr Virus ZEBRA trans-Activator

Q2 · BIOLOGY

Article

Author: Lavinia Liguori ; Romy Rothe ; Ana Villegas-Mendez ; Didier Grunwald ; Emmanuel Drouet ; Bruno Marques ; Jean-Luc Lenormand

The Epstein-Barr virus basic leucine zipper transcriptional activator ZEBRA was shown recently to cross the outer membrane of live cells and to accumulate in the nucleus of lymphocytes. We investigated the potential application of the Epstein-Barr virus trans-activator ZEBRA as a transporter protein to facilitate transduction of cargo proteins. Analysis of different truncated forms of ZEBRA revealed that the minimal domain (MD) required for internalization spans residues 170-220. MD efficiently transported reporter proteins such as enhanced green fluorescent protein (EGFP) and beta-galactosidase in several normal and tumor cell lines. Functionality of internalized cargo proteins was confirmed by beta-galactosidase activity in transduced cells, and no MD-associated cell toxicity was detected. Translocation of MD through the cell membrane required binding to cell surface-associated heparan sulfate proteoglycans as shown by strong inhibition of protein uptake in the presence of heparin. We found that internalization was blocked at 4 degrees C, whereas no ATP was required as shown by an only 25% decreased uptake efficiency in energy-depleted cells. Common endocytotic inhibitors such as nystatin, chlorpromazine, and wortmannin had no significant impact on MD-EGFP uptake. Only methyl-beta-cyclodextrin inhibited MD-EGFP uptake by 40%, implicating the lipid raft-mediated endocytotic pathway. These data suggest that MD-reporter protein transduction occurs mostly via direct translocation through the lipid bilayer and not by endocytosis. This mechanism of MD-mediated internalization is suitable for the efficient delivery of biologically active proteins and renders ZEBRA-MD a promising candidate for therapeutic protein delivery applications.

01 Nov 2006·Journal of VirologyQ2 · MEDICINE

Postentry Events Are Responsible for Restriction of Productive Varicella-Zoster Virus Infection in Chinese Hamster Ovary Cells

Q2 · MEDICINE

Article

Author: Levin, Myron J. ; Banfield, Bruce W. ; Mizokami, Kara R. ; Simpson, Scott A. ; Cai, Guang-Yun ; Finnen, Renée L. ; Pizer, Lewis I.

ABSTRACTProductive infection of varicella-zoster virus (VZV) in vitro is restricted almost exclusively to cells derived from humans and other primates. We demonstrate that the restriction of productive VZV infection in CHO-K1 cells occurs downstream of virus entry. Entry of VZV into CHO-K1 cells was characterized by utilizing an ICP4/β-galactosidase reporter gene that has been used previously to study herpes simplex virus type 1 entry. Entry of VZV into CHO-K1 cells involved cell surface interactions with heparan sulfate glycosaminoglycans and a cation-independent mannose-6-phosphate receptor. Lysosomotropic agents inhibited the entry of VZV into CHO-K1 cells, consistent with a low-pH-dependent endocytic mechanism of entry. Infection of CHO-K1 cells by VZV resulted in the production of both immediate early and late gene products, indicating that a block to progeny virus production occurs after the initiation of virus gene expression.

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