ライフサイエンスコーパス: HRD

1 HRD is always expressed in D2, but in B6, it is expresse

2 HRD patients with germline or somatic alterations in any

3 HRD was associated with higher ex vivo PARPi sensitivity

4 eived anthracycline and no radiotherapy or a HRD <0.1Gy, by 60.4 (95% CI, 22.4-163.0) in those who ha

5 ose who had received no anthracycline and an HRD>/=30Gy, and 61.5 (95% CI, 19.6-192.8) in those who h

6 e who had received both anthracycline and an HRD>/=30Gy.

7 thracycline and either no radiotherapy or an HRD<0.1Gy, the risk was multiplied by 18.4 (95% CI, 7.1-

8 dual-lumen cannula which was connected to an HRD via extracorporeal circulation.

9 Identification of EOC patients with an HRD phenotype may help tailor specific therapies.

10 Chemotherapy information was collected and HRD was estimated.

11 Both the HIP and HRD/DER pathways contribute to the degradation of CPY*,

12 e rare autosomal recessive syndrome known as HRD, a devastating disorder characterized by congenital

13 unction of the complex was observed for both HRD and DOA pathway substrates.

14 The underlying genes are called HRD (pronounced "herd"), for HMG-CoA reductase degradati

15 topic HMGR, required the function of certain HRD (HMGR degradation) and UBC genes.

16 ge, grade, and age and hazard rate of death (HRD).

17 Here we identify an HR defect (HRD) gene signature that can be used to functionally ass

18 inducing agents through their HR deficiency (HRD), BRCA1-associated tumors display heterogeneous resp

19 rs with homologous recombination deficiency (HRD) (hazard ratio, 0.38; 95% CI, 0.24 to 0.59) and 9.3

20 valuated homologous recombination deficient (HRD) phenotypes in epithelial ovarian cancer (EOC) consi

21 s of the homologous recombination-deficient (HRD) status on the clinicopathologic features, chemother

22 embrane-bound HMG-CoA reductase degradation (HRD) ubiquitin-ligase complex is a key player of the ER-

23 Human remains detection (HRD) canines utilize this odor signature to locate human

24 that the conserved UBN1 Hpc2-related domain (HRD) is a novel H3.3-specific-binding domain.

25 lationship between the heart radiation dose (HRD) received during childhood and the risk of CD.

26 11 in S. cerevisiae is independent of either HRD or UBC gene function, but it is largely dependent on

27 ing a BRCA1/2 mutation, but with an elevated HRD-LOH score, who achieved a favorable pathologic respo

28 ane protein Hrd3, which is also required for HRD-dependent degradation.

29 ency was assessed by loss of heterozygosity (HRD-LOH) in pretreatment core breast biopsies.

30 bone geometry of the catalytically important HRD motif deviates from ideality in high-resolution stru

31 igated Usa1p to understand its importance in HRD complex action.

32 ed the Hmg-CoA reductase degradation ligase (HRD-ligase), and degraded by cytosolic 26S proteasomes.

33 and two of them had increased tumor HRD-LOH/HRD-LST scores.

34 iency-large-scale state transitions [HRD-LOH/HRD-LST] scores were 12.68 and 5.11, respectively), wher

35 Mean HRD-LOH scores were higher in responders compared with n

36 as a unique mechanism that rescues a mutant HRD allele by producing a functional TBCE protein.

37 typically as important as Hrd1 in the native HRD complex.

38 Hmg2p degradation occurs by the action of HRD genes that direct Hmg2p to the ubiquitin-proteasome

39 Clearly, DNA methylation of HRD precedes chromatin compaction and loss of expression

40 Regulation of HRD-dependent Hmg2p degradation appears to occur by the

41 Our data indicated that the role of HRD genes in protein degradation, even in this highly de

42 he presence or absence of gBRCA mutations or HRD status, with moderate bone marrow toxicity.

43 appears that the physiologically regulated, HRD-dependent degradation of HMGR is effected by a progr

44 tly examined the association of the separate HRD complex components with various ERAD substrates.

45 n the F-helix hydrogen bonds to the strained HRD backbone in diverse eukaryotic and eukaryotic-like p

46 We therefore suggest that HRD as predicted by a functional RAD51 assay correlates

47 The HRD (HMG-CoA reductase degradation) pathway is a conserv

48 The HRD complex engages in lumen to cytosol communication re

49 The HRD in C2 also decreased compared with C1, although to a

50 The HRD is capable of reversal of anticoagulation following

51 The HRD pathway is a conserved route of ubiquitin-dependent,

52 The HRD phenotype was most common in high grade serous EOC.

53 The HRD run time averaged 27.4 +/-1.5 mins targeted to remov

54 The HRD run time was determined by a previously established

55 The HRD, therefore, can serve as an alternative to achieve h

56 The HRD-LOH assay was able to identify patients with sporadi

57 Because the HRD genes were required for the degradation of both regu

58 binations of compounds are recognized by the HRD canines.

59 east HMG-CoA reductase (Hmg2p) occurs by the HRD endoplasmic reticulum quality control pathway, imply

60 ted endoplasmic reticulum degradation by the HRD pathway.

61 tested this model by directly comparing the HRD dependency of the ER-associated degradation for vari

62 nregulated substrates of ER degradation, the HRD genes are the agents of HMG-R degradation but not th

63 erevisiae that functions separately from the HRD/DER pathway comprised of Hrd1p, Hrd3p, Der1p, and Ub

64 the strain because of a peptide flip in the HRD backbone.

65 w-up duration was 14 months; patients in the HRD group had lower tumor progression rates at 6 months,

66 ation of HIP substrates does not involve the HRD/DER pathway ubiquitin ligase Hrd1p, but instead uses

67 erized quality control ubiquitin ligase, the HRD complex, which is responsible for the endoplasmic re

68 Moreover, the HRD gene signature serves as an effective drug discovery

69 through the plasma separation chamber of the HRD (where heparin was bound to PLL), and reinfused into

70 support the model of a dimeric state of the HRD complex and provide first-time evidence of self-asso

71 er binding to Hrd3, another component of the HRD complex.

72 ino acid residues and on the function of the HRD genes.

73 volved in the function and regulation of the HRD pathway of ERAD.

74 At the end of the HRD run, heparin concentration decreased to 0.51+/-0.09

75 Usa1p is a recently discovered member of the HRD ubiquitin ligase complex.

76 Use of the HRD was not associated with any adverse hemodynamic reac

77 rane protein Der1, which is a subunit of the HRD-ligase, is involved in the export of aberrant polype

78 ned before, during, and after the use of the HRD.

79 Compared with HR-competent patients, the HRD group was predominantly serous with a higher median

80 CPY* overexpression likely saturates the HRD/DER pathway and activates the HIP pathway, so the sl

81 uch as the hydrophobic regulatory spine, the HRD motif, and the electrostatic switch.

82 as led to the reasonable hypothesis that the HRD (Hmg CoA reductase degradation) gene-encoded protein

83 nzyme A reductase (HMGR), indicated that the HRD complex discerns between a degradation-competent "mi

84 We have discovered that the HRD ubiquitin ligase complex associates with both ERAD s

85 om those of Der1p, which is recruited to the HRD complex by Usa1p.

86 These data favor models in which the HRD gene-encoded proteins function as specificity factor

87 More importantly, this HRD gene signature is able to predict clinical outcomes

88 By using this HRD gene signature as a functional network analysis tool

89 s) BRCA1 protein that mediated resistance to HRD-targeted therapies.

90 a1185stop tumors responded markedly worse to HRD-targeted therapy than did Brca15382stop tumors.

91 in-specific DNA methylation of the transgene HRD.

92 on deficiency-large-scale state transitions [HRD-LOH/HRD-LST] scores were 12.68 and 5.11, respectivel

93 tations, and two of them had increased tumor HRD-LOH/HRD-LST scores.

94 veal that conserved residues within the UBN1-HRD and H3.3 G90 as key determinants of UBN1-H3.3-bindin

95 emical and biophysical studies show the UBN1-HRD preferentially binds H3.3/H4 over H3.1/H4.

96 ompared prospectively in HR-competent versus HRD patients.