ライフサイエンスコーパス: Sasa

1 us proteins, including KaiA, KaiB, KaiC, and SasA.

2 40H) x Ade(a) and E(40H) x Ade(s), have zero SASA.

3 SasA, a circadian clock-output protein, binds to the CI

4 SasA, a clock-associated histidine kinase, is necessary

5 SasA acts as a kinase toward RpaA, whereas CikA, previou

6 N-SasA adopts a canonical thioredoxin fold but lacks the c

7 Because the clock output protein SasA also binds to CI and competes with KaiB for binding

8 lated by two antagonistic histidine kinases, SasA and CikA, which are sequentially activated at disti

9 eins and a set of output signaling proteins, SasA and CikA, which transduce this rhythm to control ge

10 he mutually antagonistic signaling proteins, SasA and CikA.

11 ts that the structural differences between N-SasA and KaiB are the result of only a few critical amin

12 e no clear details to suggest competition of SasA and KaiB for KaiC binding.

13 N-SasA and KaiB share significant sequence similarity and,

14 Here, we report the NMR structure of N-SasA and show it to be different from that of KaiB.

15 ve time, communicate temporal information to SasA, and may control access to promoter elements by imp

16 Solvent accessible surface area (SASA) calculations on all the five MD structures shows t

17 output-independent pathway, suggesting that SasA can influence entrainment through direct interactio

18 lfactory epithelium (SORB, SORF, all SVR and Sasa CaSR sequences), testis (SORB, SORD and Sasa CaSR)

19 Sasa CaSR sequences), testis (SORB, SORD and Sasa CaSR) and/or anterior kidney (SORB and Sasa CaSR).

20 Sasa CaSR) and/or anterior kidney (SORB and Sasa CaSR).

21 A family of sequences (Sasa CaSR1-6), isolated using the same degenerate primer

22 iate global transcription via output factors SasA, CikA, LabA, RpaA, and RpaB.

23 show that KaiB and the clock-output protein SasA compete for overlapping binding sites, which includ

24 have an alternating pattern of high and low SASA consistent with a beta strand structure.

25 CikA and SasA cooperate to generate an oscillation of RpaA activi

26 In 2001, Hatano and Sasa derived a testable prediction of this theory.

27 query according to amino acids, buried area (SASA), energy or keywords related to indication areas, e

28 We suggest that this surface is used by N-SasA for protein-protein interactions.

29 (beta), and solvent accessible surface area (SASA, gamma) terms.

30 hose in the previously reported trees of the sasA gene and the kaiBC operon, two other elements of th

31 (PCC 7942) the kai genes A, B, and C and the sasA gene encode the functional protein core of the timi

32 ions in the Synechococcus adaptive sensor A (sasA) gene that produce nearly WT rhythms of gene expres

33 The ability of <SASA> data from HR-HRPF to differentiate molecular model

34 ality was found to be comparable to that of <SASA> data obtained from X-ray crystal structures, indic

35 oreover, we demonstrated the ability to use <SASA> measurements from HR-HRPF to differentiate molecul

36 The accuracy of the resulting <SASA> measurements was tested by using well-characterize

37 te average solvent accessible surface area (<SASA>) of amino acid side chains.

38 ctions as the sensory domain controlling the SasA histidine kinase activity.

39 The N-terminal domain of SasA (N-SasA) interacts directly with KaiC and likely functions

40 tral timing mechanism, and the sensor kinase SasA is a primary transducer of temporal information.

41 Although sasA is required for global gene expression rhythmicity,

42 shares a sequence-homologous domain with the SasA kinase.

43 Mutations in the sasA locus cause defective fruiting body formation, redu

44 The wild-type sasA locus has been located on a 14-kb cloned fragment o

45 A wild-type sasA locus is critical for Myxococcus xanthus multicellu

46 These data indicate that the sasA locus is required for the biosynthesis of O-antigen

47 s genes are similar to those of the original sasA locus mutants.

48 nce of a 7-kb region containing the complete sasA locus was determined.

49 and sporulation result from mutations in the sasA locus, which encodes the wzm wzt wbgA (formerly rfb

50 Mutants carrying these same sasA mutations are defective in social motility and form

51 The N-terminal domain of SasA (N-SasA) interacts directly with KaiC and likely fu

52 ibited a degree of correlation with the mean SASA of whole residues within each peptide segment, HDX

53 uantify the solvent accessible surface area (SASA) of beta1 strand residues in the GABAA beta3 homope

54 ctions, the solvent accessible surface area (SASA) of the ligands, and stabilization of key structura

55 The solvent accessible surface area (SASA) of the polypeptide chain plays a key role in prote

56 ly more active than expected from either the SASA or hydrogen bonding status of the exchangeable amid

57 by the Kai proteins on the rate at which the SasA protein autophosphorylates.

58 nmentally sensitive NblS-RpaB system and the SasA-RpaA clock output system integrate relevant extra-

59 The SasA-RpaA two-component system constitutes a key output

60 onequilibrium systems, supporting Hatano and Sasa's proposed extension of thermodynamics to arbitrary

61 assembly sites (S. aureus surface protein A (SasA), SasD, SasF and SasK) do not.

62 inning of rfbA, produced less O-antigen than sasA+ strains.

63 Furthermore, the expression of both fdgA and sasA was partially dependent on the C-signal.

64 required for the developmental expression of sasA, which is also involved in the biosynthesis of the