1 ein (gp170) that is further modified into an endo H-resistant glycoprotein (gp180) in the Golgi appar

2 o-N-acetlyglucosaminidases (e.g., endo-F and endo-H), which respectively cleave between the GlcNAc&bo

3                                      Because endo-H sensitivity is tightly correlated with endoplasmi

4 endo H-resistant in untreated cells, becomes endo H-sensitive following ICZ treatment.

5 nsitive to treatment with endoglycosidase H (endo H), while the mature gCIII complex was essentially

6 s newly synthesized as an endoglycosidase H (endo H)-sensitive glycoprotein (gp170) that is further m

7 ce TPO molecules remained endoglycosidase H (endo H)-sensitive.

8  cd81(-/-) B cells and is endoglycosidase H (endo-H) resistant.

9                           Endoglycosidase H (endo-H) treatment of particles demonstrated that the inc

10                  This glycoprotein, which is endo H-resistant in untreated cells, becomes endo H-sens

11 in cd81(-/-) and in wild-type B cells and is endo-H sensitive.

12  thyrocyte cell line also exhibits almost no endo H-resistant TPO, much of the endogenous rTPO is loc

13 e thyroid tissue TPO also shows little or no endo H resistance, although cell fractionation still nee

14   Both inhibitors retarded the maturation of endo-H-resistant forms of murine and human class I molec

15 actacystin did not inhibit the maturation of endo-H-resistant forms of Qa-1b that are dependent on th

16        The 25-kDa intermediate was partially endo H-sensitive, colocalized with the medial Golgi resi

17 urine and human class I molecules from their endo-H-sensitive precursors in cell lines with functiona

18 s on the 100-kDa form of gO were modified to endo H-resistant states as the 125-kDa gO formed, additi

19 TPP I was found to be partially resistant to endo H treatment; thus, some of its N-linked oligosaccha

20                       TcAQP was sensitive to endo H treatment, suggesting that the protein is N-glyco

21 ast, the majority of the incorporated E2 was endo-H resistant.