ライフサイエンスコーパス: TC-II

1 TC II-R delivered to the BLM during this period was prog

2 ibited the intracellular degradation of 125I-TC II, which resulted in secretion of 60-65% of TC II-Cb

3 ral transcytosis of either [57Co]Cbl or 125I-TC II.

4 When 125I-TC II-Cbl was orally administered to rats, intact labele

5 of these cells, and in polarized cells via a TC II receptor expressed in the basolateral membranes.

6 n up from the circulation by all cells via a TC II receptor expressed in the plasma membrane of these

7 pathways of internalized Cbl bound to IF and TC II in polarized epithelial cells; and (c) the absorpt

8 pects of Cbl binding protein ligands, IF and TC II, and their cell-surface receptors, IF-Cbl receptor

9 cell-surface receptors, IF-Cbl receptor and TC II receptor; (b) the cellular sorting pathways of int

10 nternalized and subsequently transcytosed as TC II-Cbl.

11 cognized non-lysosomal pathway in which both TC II and Cbl are transcytosed and (b) basolateral side

12 effect on either total cellular cholesterol, TC II-R activity, or PL levels.

13 62 kDa) and the enzymatically deglycosylated TC II-R (45-47 kDa) demonstrated optimal association and

14 he higher order of the BLM, is essential for TC II-R dimerization.

15 retained by the cells, but transferred from TC II to other cellular proteins.

16 Holo-TC II is also the form in which absorbed cobalamin enter

17 Holo-TC II, which correlated directly with cobalamin and inve

18 to transcobalamin II (TC II), known as holo-TC II, is the active cobalamin fraction taken up by tiss

19 The influences on holo-TC II are complex and require careful analysis.

20 metabolic and absorptive influences on holo-TC II.

21 Serum holo-TC II and indexes of cobalamin metabolism in 23 treated

22 Serum holo-TC II cannot be used clinically to diagnose cobalamin ma

23 status is a major determinant of serum holo-TC II.

24 Therefore, holo-TC II has been proposed variously as a marker of cobalam

25 Transcobalamin II (TC II) receptor is expressed in the apical and basolater

26 nking region of the human transcobalamin II (TC II) transfected in human intestinal epithelial Caco-2

27 Cobalamin attached to transcobalamin II (TC II), known as holo-TC II, is the active cobalamin fra

28 concentrations (10(-6) M) of NEM resulted in TC II-R exhibiting a loss of ligand binding and an incre

29 embranes revealed similar amounts of 124-kDa TC II-R dimer protein.

30 ified 72-kDa TC II-R, like the native 62-kDa TC II-R in untreated cells, turned over rapidly with a t

31 on with N-ethylmaleimide (NEM) of the 62-kDa TC II-R monomer in vitro or treatment of human intestina

32 methionine revealed that the modified 72-kDa TC II-R, like the native 62-kDa TC II-R in untreated cel

33 Labeled 72-kDa TC II-R, which was retained intracellularly following tr

34 orally administered to rats, intact labeled TC II was detected in the portal blood 4 and 8 h later.

35 5 degrees C) 30 and 180 fmol of the ligand, TC II-[57Co]cobalamin (Cbl), to the apical and the basol

36 Mature TC II-R dimerized upon insertion into synthetic phosphat

37 Both the mature TC II-R (62 kDa) and the enzymatically deglycosylated TC

38 II, which resulted in secretion of 60-65% of TC II-Cbl complex into the basolateral medium.

39 GC/GT box and the weak promoter activity of TC II is due to the transcriptional repression caused by

40 tenance of intramolecular disulfide bonds of TC II-R is important for its acquisition of ligand bindi

41 Dimerization of TC II-R also occurred with vesicles prepared using lipid

42 hese results we suggest that dimerization of TC II-R is mediated by its interactions with a rigid mor

43 hatidylcholine revealed that interactions of TC II-R with PC vesicles increased order around the prob

44 -treated filter-grown cells revealed loss of TC II-R but not cation-independent mannose 6-phosphate r

45 were carried out to define the mechanism of TC II-R dimerization.

46 p3 repressed Sp1-mediated transactivation of TC II transcription.

47 ffected rabbit serum inhibited the uptake of TC II-[57Co]cobalamin (Cbl) from the basolateral side of

48 inhibited the binding of the ligand to pure TC II-R and the harvested affected rabbit serum inhibite

49 membranes, respectively, and in vitro, pure TC II-R monomer dimerizes upon insertion into egg PC/cho

50 complete loss of transcobalamin II receptor (TC II-R) activity/protein levels in the BLM and the disa

51 Transcobalamin II receptor (TC II-R) exists as a monomer and a dimer of molecular ma

52 Transcobalamin II-receptor (TC II-R) contains 10 half-cysteines, of which 8 are invo

53 human placental transcobalamin II-receptor (TC II-R) failed to thrive with no apparent tissue or org

54 l epithelial Caco-2 cells have revealed that TC II promoter activity is: (a) very weak; (b) restricte

55 These studies suggest that TC II-Cbl is processed when presented to the (a) apical/

56 that tissue/cell specific expression of the TC II gene may be controlled by the relative ratios of S

57 s, we suggest that circulatory antibodies to TC II-R cause its in vivo functional inactivation, suppr

58 teral side by the lysosomal pathway in which TC II is degraded and the released Cbl is utilized.