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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                         Human cyclophilin B (CypB) is oversecreted by pancreatic cancer cells, making
8          Here, we report that cyclophilin B (CypB), a prolyl isomerase residing in the endoplasmic re
9 nteraction with its cofactor, cyclophilin B (CypB), even though the I432V mutation is located outside
10 o identify the M9-5 target as cyclophilin B (CypB).
11  triple helix is catalyzed by cyclophilin B (CypB).
12 tilage-associated protein and cyclophilin B (CypB).
13     A direct, functional interaction between CypB (which possesses peptidyl-prolyl cis-trans isomeras
14 erent protein networks that were impacted by CypB knockdown.
15 howed that 663 transcripts were regulated by CypB knockdown, and that many of these gene products con
16                               The P3H1.CRTAP.CypB complex also delayed the in vitro fibril formation
17 s isomerase activity and that the P3H1.CRTAP.CypB complex has another important function: it acts as
18                               The P3H1.CRTAP.CypB complex inhibited the thermal aggregation of citrat
19                     As keratinocytes express CypB receptors (CD147) and CypB exhibits chemotactic pro
20                                     Finally, CypB knock-out mice were found to have reduced ADAMTS13
21 , which could impede the use of aptamers for CypB detection.
22 ion-based strategy simultaneously identified CypB as a serum biomarker and generated a new reagent to
23                              To establish if CypB can hydrolyze electrode-bound nucleic acids, we use
24 emonstrated a highly significant increase in CypB protein levels as a function of breast cancer progr
25 , and abnormal unfolded protein responses in CypB-depleted glioblastoma multiforme cells indicated th
26 ying oncogenic transformation, and they make CypB an attractive and immediately targetable molecule f
27 d to develop aptamer-based assays to measure CypB levels in biofluids.
28 sensitive electrochemical sensors to measure CypB's hydrolytic activity.
29 l cis-trans isomerase activity of the mutant CypB is normal when analyzed in vitro.
30 creased the mobility of CypB(WT)-GFP but not CypB(W128A)-GFP.
31                        Future development of CypB bioassays will require the use of nuclease-resistan
32 ypB with alanine resulted in dissociation of CypB(W128A)-green fluorescent protein (GFP) from the ER.
33 at the side opposite the catalytic domain of CypB.
34 of multiple oncogenic proteins downstream of CypB may thus contribute to the poor outcome of glioblas
35 ults suggest that the enhanced expression of CypB in malignant breast epithelium may contribute to th
36  To better understand the global function of CypB in breast cancer, T47D cells with a small interferi
37 ly, depletion or pharmacologic inhibition of CypB caused hyperactivation of the oncogenic RAS-mitogen
38           We found that CsA, an inhibitor of CypB, reduces the secretion of ADAMTS13 and leads to con
39  small interfering RNA-mediated knockdown of CypB were generated.
40 g immunoprecipitation and siRNA knockdown of CypB.
41 cant reduction in the diffusible mobility of CypB(W128A)-GFP compared with CypB(WT)-GFP, consistent w
42  CsA significantly decreased the mobility of CypB(WT)-GFP but not CypB(W128A)-GFP.
43 B(WT)-GFP, consistent with redistribution of CypB(W128A)-GFP into secretory vesicles disconnected fro
44 A-binding site of CypB controls retention of CypB within the ER and regulates entry into the secretor
45  concentrations of CsA regulate secretion of CypB by keratinocytes, and that a key residue within the
46 s as low as 1 pM of CsA induced secretion of CypB.
47 a key residue within the CsA-binding site of CypB controls retention of CypB within the ER and regula
48 ophan residue 128 in the CsA-binding site of CypB with alanine resulted in dissociation of CypB(W128A
49                 We found that suppression of CypB reduced cell proliferation and survival in human gl
50  proteins, such as the formation of the P3H1.CypB.cartilage-associated protein complex, resulting in
51  mutation is located outside of the reported CypB binding site (amino acids 520 to 591).
52 erone receptor were all down-regulated in si-CypB cells.
53  proteins, we unequivocally demonstrate that CypB can cleave nucleic acids.
54          Functional assays demonstrated that CypB knockdown also decreased cell growth, proliferation
55 glioblastoma multiforme cells indicated that CypB alleviates oxidative and ER stresses and coordinate
56 s of gene expression databases revealed that CypB is upregulated in many cases of malignant glioma.
57            Using brefeldin A, we showed that CypB is secreted from keratinocytes via the constitutive
58       We report that as in other cell types, CypB trafficked from the ER and was secreted by keratino
59 le mobility of CypB(W128A)-GFP compared with CypB(WT)-GFP, consistent with redistribution of CypB(W12
60                Challenging such sensors with CypB and control proteins, we unequivocally demonstrate