heparin/sarcoma

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The Kaposi's sarcoma-associated herpesvirus complement control protein (KCP) binds to heparin and cell surfaces via positively charged amino acids in CCP1-2.

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The Kaposi's sarcoma-associated herpesvirus (KSHV) complement control protein (KCP) inhibits the human complement system, and is similar in structure and function to endogenous complement inhibitors. Other inhibitors such as C4b-binding protein and factor H, as well as the viral homologue vaccinia

The heparin binding proteins of sarcoma induced by methylcholantrene in rats.

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The proteins binding and neutralizing the heparin of sarcoma induced by methylcholantrene are basic proteins. They are a mixture of at least three different proteins, possessing cathodic mobility in polyacrylamide gel electrophoresis of pH 2.7 and having a low molecular weight.

Immunolocalization of heparin-binding EGF-like growth factor (HB-EGF) as a possible immunotarget in diagnosis of some soft tissue sarcomas.

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Heparin-binding EGF-like growth factor (HB-EGF), a member of the family of epidermal growth factors (EGFs), is involved in several biological processes and tumor formation. Several lines of evidence show that HB-EGF plays a key role in the acquisition of malignant phenotype. Studies show that HB-EGF

Supersulfated low-molecular weight heparin synergizes with IGF1R/IR inhibitor to suppress synovial sarcoma growth and metastases.

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Synovial sarcoma (SS) is an aggressive tumor with propensity for lung metastases which significantly impact patients' prognosis. New therapeutic approaches are needed to improve treatment outcome. Targeting the heparanase/heparan sulfate proteoglycan system by heparin derivatives which act as

Apolipoprotein E (ApoE), a novel heparin-binding protein inhibits the development of Kaposi's sarcoma-like lesions in BALB/c nu/nu mice.

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Recombinant apolipoprotein E-3 (ApoE-3), expressed in Escherichia coli, was purified and used in an in vitro and an in vivo model system for acquired immunodeficiency syndrome-associated Kaposi's sarcoma (AIDS-KS). This protein blocked cell proliferation and chemotaxis of AIDS-KS cells in response

Inhibitory effect of heparin on Rous sarcoma virus.

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[Action of heparin and other substances on sarcoma 180].

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THE ACTION OF HEPARIN IN VITRO ON SYRIAN-HAMSTER SARCOMA-CELL CULTURES.

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Inhibition of deoxynucleotide-polymerizing enzyme activities of human cells and of simian sarcoma virus by heparin.

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HIV-tat protein is a heparin-binding angiogenic growth factor.

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Transgenic animal studies have linked the expression of the HIV-1 tat gene to the appearance of Kaposi's sarcoma (KS)-like lesions. We have recently shown that recombinant tat is angiogenic in vivo, and that tat angiogenic response is enhanced by heparin. Also in the rabbit cornea model, recombinant

Treatment of autochthonous rat brain tumors with steroid plus heparin: a brief report.

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Treatment of rats bearing intracranial gliomas induced by the avian sarcoma virus with heparin plus steroid has failed to effectively extend survival time.

Purification of reverse transcriptase from avian retroviruses using affinity chromatography on heparin-sepharose.

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Reverse transcriptase from Rous sarcoma virus and avian myeloblastosis virus was purified by a rapid two-step procedure using chromatography on phosphocellulose and heparin-Sepharose. The resulting enzyme was homogeneous, had a high specific activity and was free of contaminating nucleases. This

A retinoic acid responsive gene, MK, produces a secreted protein with heparin binding activity.

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MK is a gene whose expression increases transiently during retinoic acid-induced differentiation of embryonal carcinoma cells. MK polypeptide was secreted by differentiating HM-1 embryonal carcinoma cells and by L-cells transfected with an MK cDNA under the control of the beta-actin promoter and

Heparin-treated, v-myc-transformed chicken heart mesenchymal cells assume a normal morphology but are hypersensitive to epidermal growth factor (EGF) and brain fibroblast growth factor (bFGF); cells transformed by the v-Ha-ras oncogene are refractory to EGF and bFGF but are hypersensitive to insulin-like growth factors.

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Chicken heart mesenchymal cells do not proliferate in culture medium containing heat-defibrinogenated plasma but proliferate briskly when incubated with epidermal growth factor (EGF) or brain fibroblast growth factor (bFGF) plus insulin-like growth factors (IGFs) or when infected with sarcoma or

Heparin-binding epidermal growth factor-like growth factor, a v-Jun target gene, induces oncogenic transformation.

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Jun is a transcription factor belonging to the activator protein 1 family. A mutated version of Jun (v-Jun) transduced by the avian retrovirus ASV17 induces oncogenic transformation in avian cell cultures and sarcomas in young galliform birds. The oncogenicity of Jun probably results from

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