ライフサイエンスコーパス: CypB

1 tinocytes express CypB receptors (CD147) and CypB exhibits chemotactic properties, these data have im

2 sue microarray that was labeled with an anti-CypB antibody demonstrated a highly significant increase

3 e evidence demonstrating that cyclophilin B (CypB) activity plays an important role in the secretion

4 sociated protein (CRTAP), and cyclophilin B (CypB) can be isolated from chick embryos on a gelatin-Se

5 Cyclophilin B (CypB) is a 21-kDa protein with peptidyl-prolyl cis-trans

6 Cyclophilin B (CypB) is an endoplasmic reticulum (ER)-resident member o

7 Here, we report that cyclophilin B (CypB), a prolyl isomerase residing in the endoplasmic re

8 nteraction with its cofactor, cyclophilin B (CypB), even though the I432V mutation is located outside

9 o identify the M9-5 target as cyclophilin B (CypB).

10 triple helix is catalyzed by cyclophilin B (CypB).

11 tilage-associated protein and cyclophilin B (CypB).

12 A direct, functional interaction between CypB (which possesses peptidyl-prolyl cis-trans isomeras

13 erent protein networks that were impacted by CypB knockdown.

14 howed that 663 transcripts were regulated by CypB knockdown, and that many of these gene products con

15 The P3H1.CRTAP.CypB complex also delayed the in vitro fibril formation

16 s isomerase activity and that the P3H1.CRTAP.CypB complex has another important function: it acts as

17 The P3H1.CRTAP.CypB complex inhibited the thermal aggregation of citrat

18 As keratinocytes express CypB receptors (CD147) and CypB exhibits chemotactic pro

19 Finally, CypB knock-out mice were found to have reduced ADAMTS13

20 ion-based strategy simultaneously identified CypB as a serum biomarker and generated a new reagent to

21 emonstrated a highly significant increase in CypB protein levels as a function of breast cancer progr

22 , and abnormal unfolded protein responses in CypB-depleted glioblastoma multiforme cells indicated th

23 ying oncogenic transformation, and they make CypB an attractive and immediately targetable molecule f

24 l cis-trans isomerase activity of the mutant CypB is normal when analyzed in vitro.

25 creased the mobility of CypB(WT)-GFP but not CypB(W128A)-GFP.

26 ypB with alanine resulted in dissociation of CypB(W128A)-green fluorescent protein (GFP) from the ER.

27 at the side opposite the catalytic domain of CypB.

28 of multiple oncogenic proteins downstream of CypB may thus contribute to the poor outcome of glioblas

29 ults suggest that the enhanced expression of CypB in malignant breast epithelium may contribute to th

30 To better understand the global function of CypB in breast cancer, T47D cells with a small interferi

31 ly, depletion or pharmacologic inhibition of CypB caused hyperactivation of the oncogenic RAS-mitogen

32 We found that CsA, an inhibitor of CypB, reduces the secretion of ADAMTS13 and leads to con

33 small interfering RNA-mediated knockdown of CypB were generated.

34 g immunoprecipitation and siRNA knockdown of CypB.

35 cant reduction in the diffusible mobility of CypB(W128A)-GFP compared with CypB(WT)-GFP, consistent w

36 CsA significantly decreased the mobility of CypB(WT)-GFP but not CypB(W128A)-GFP.

37 B(WT)-GFP, consistent with redistribution of CypB(W128A)-GFP into secretory vesicles disconnected fro

38 A-binding site of CypB controls retention of CypB within the ER and regulates entry into the secretor

39 concentrations of CsA regulate secretion of CypB by keratinocytes, and that a key residue within the

40 s as low as 1 pM of CsA induced secretion of CypB.

41 a key residue within the CsA-binding site of CypB controls retention of CypB within the ER and regula

42 ophan residue 128 in the CsA-binding site of CypB with alanine resulted in dissociation of CypB(W128A

43 We found that suppression of CypB reduced cell proliferation and survival in human gl

44 proteins, such as the formation of the P3H1.CypB.cartilage-associated protein complex, resulting in

45 mutation is located outside of the reported CypB binding site (amino acids 520 to 591).

46 erone receptor were all down-regulated in si-CypB cells.

47 Functional assays demonstrated that CypB knockdown also decreased cell growth, proliferation

48 glioblastoma multiforme cells indicated that CypB alleviates oxidative and ER stresses and coordinate

49 s of gene expression databases revealed that CypB is upregulated in many cases of malignant glioma.

50 Using brefeldin A, we showed that CypB is secreted from keratinocytes via the constitutive

51 We report that as in other cell types, CypB trafficked from the ER and was secreted by keratino

52 le mobility of CypB(W128A)-GFP compared with CypB(WT)-GFP, consistent with redistribution of CypB(W12