ライフサイエンスコーパス: non-fibrillar

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1 gen occurs in two major forms: fibrillar and non-fibrillar.

2 Our results suggest that the ability of non-fibrillar Abeta oligomers to interact with and disru

3 This suggests that non-fibrillar Abeta or early stage plaque depostion migh

4 r's plaque peptide Abeta(1-40), as well as a non-fibrillar aggregate induced by Zn(2+).

5 f the monomer and the hairpin assembles into non-fibrillar aggregates, demonstrating that the hairpin

6 associate with themselves to form larger but non-fibrillar aggregates.

7 to be the arrest of aggregation in an early, non-fibrillar aggregation stage.

8 but also rescues proteins from irreversible non-fibrillar aggregation.

9 These data suggest that soluble non-fibrillar amyloid may contribute to the pathogenesis

10 Recently it has been demonstrated that non-fibrillar assemblies of A beta possess electrophysio

11 It is increasingly recognized that small non-fibrillar beta-sheet-rich oligomers of PrP may be of

12 Collagen XV (COLXV) is a secreted non-fibrillar collagen found within basement membrane (B

13 e amino acid sequence of type VI collagen, a non-fibrillar collagen that forms antiparallel dimers.

14 which encodes the alpha chain of an atypical non-fibrillar collagen with a single transmembrane domai

15 Non-fibrillar collagens are structurally more variable a

16 are found in the triple-helix domains of all non-fibrillar collagens, and perturbations to the triple

17 ound normally in the triple helix domains of non-fibrillar collagens, such as type IV collagen in bas

18 in the -Gly-X-Y- repeating pattern found in non-fibrillar collagens.

19 nts may be common aggregation motifs for the non-fibrillar collagens.

20 analyzed alleles of candidate genes encoding non-fibrillar components of TTR amyloid deposits and a m

21 FBD brains has shown the presence of ABri as non-fibrillar deposits as well as amyloid fibrils.

22 y into amyloid structures while MHP1 forms a non-fibrillar film.

23 Growing evidence suggests water-soluble, non-fibrillar forms of amyloid-beta protein (Abeta) have

24 Using immunogold electron microscopy, non-fibrillar forms of PrP(d) were shown to accumulate m

25 Serum amyloid P component (SAP) is a non-fibrillar glycoprotein belonging to the pentraxin fa

26 that the cellular fibrillation also involves non-fibrillar intermediate species, and the microtubule-

27 choring directs the assembly of Sup35NM into non-fibrillar, membrane-bound aggregates that resemble P

28 infected hosts, PrPSc usually accumulates as non-fibrillar, membrane-bound aggregates.

29 uctural analyses indicate that despite their non-fibrillar morphology, the metastable Zn(2+)-Abeta40

30 These findings provide evidence that non-fibrillar oligomeric species are likely to play a cr

31 Moreover, we report the novel findings that non-fibrillar oligomeric species of ABri are more toxic

32 es suggest that increased propensity to form non-fibrillar oligomers is the shared property of these

33 Recent studies have implicated non-fibrillar oligomers of the amyloid beta (Abeta) pept

34 nsists of mineralized collagen fibrils and a non-fibrillar organic matrix, which acts as a 'glue' tha

35 These results suggest that non-fibrillar particles, with masses equivalent to 14-28

36 are either absent or present only as diffuse non-fibrillar plaques in the brain parenchyma.

37 er, all amyloid deposits contain the normal, non-fibrillar plasma glycoprotein, serum amyloid P compo

38 symmetry, which are efficient inhibitors of non-fibrillar protein aggregation.

39 partitioning to a faster pathway leading to non-fibrillar self-associated aggregates at higher prote

40 Non-fibrillar soluble oligomeric forms of amyloid-beta p

41 s both the small aggregate fractions contain non-fibrillar spherical aggregates with distinct size di

42 he increased size, the protofibrils remained non-fibrillar, suggesting that the deposition of the pro

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