Words similar to ph-
Example sentences for: ph-
How can you use “ph-” in a sentence? Here are some example sentences to help you improve your vocabulary:
The Ph-SAM polymer is quite similar to the TEL-SAM polymer even though the proteins have an unrelated domain structure and show less than 20% sequence identity between the SAM domains.
Whether these TGF-β1-induced proteins restrict the ability of PH-20 to increase TNF cytotoxicity is unknown.
The Sperm Adhesion Molecule 1 (SPAM1 or PH-20) is a glycosyl-phosphatidylinositol (GPI)-linked protein found on all mammalian spermatozoa that have been examined, and has been reported to play multiple roles in fertilization [ 1 ] . Although a recent gene targeting study indicates that in mice, which have four active non-somatic hyaluronidases, Spam1 is not essential for fertilization [ 2 ] ; this is unlikely to be the case in humans where SPAM1 is the only such hyaluronidase present.
TGF-β family proteins, including β1,β2 and β3, induce TNF-resistance and suppress the PH-20 effect of increasing TNF cytotoxicity in murine L929 fibroblasts [ 8 11 ] . TGF-β1 induces a novel extracellular matrix protein that prevents TNF-mediated cell death and blocks the activation of extracellular signal-regulated kinase (ERK; also known as p42/44 mitogen-activated protein kinase, p42/44 MAPK) in L929 cells [ 8 12 ] . Additionally, TGF-β1 induces the expression of TIAF1 (TGF-β-induced antiapoptotic factor) [ 13 ] and TIF2 (TGF-β-induced factor 2) [ 14 ] that inhibit TNF cytotoxicity.
These observations are consistent with our previous finding that exogenous bovine testicular hyaluronidase PH-20 enhances TNF cytotoxicity in various cancer cells, and that TGF-β1 blocks the increased TNF cytotoxicity [ 8 15 ] . As summarized in the Figure 8, the underlying mechanisms whereby Hyal-2 induces TNF cytotoxicity appear to be associated with 1) Hyal-2 induction of the proapoptotic WOX1, 2) Hyal-2 migration to the mitochondria during apoptosis, and 3) the prolonged period of IκBα degradation and NF-κB activation in TNF-treated Hyal-2-expressing cells.
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