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1 rsors during maturation of the host protein (extein).
2 itant ligation of the flanking polypeptides (exteins).
3 ocess ligate the flanking protein sequences (exteins).
4 e joining of the flanking protein sequences (exteins).
5 rmophilic Pyrococcus abyssi PolII intein and extein.
6 s cleavage of the intein from its N-terminal extein.
7 ptide bond cleavage between the intein and C-extein.
8  intein, is removed from a host protein, the extein.
9 in level from the flanking host protein, the exteins.
10 oncomitant with the specific ligation of the exteins.
11 rm a native peptide bond between the ligated exteins.
12 y 100 amino acids long, fused to appropriate exteins.
13 er native conditions was achieved using mini exteins.
14 five mutations at the first residue of the C-extein (+1), and describe molecular properties that may
15  conditions, and ectopic expression of Mtb N-extein activated LexA in E. coli.
16 rmation of a thioester linkage between the N-extein and intein.
17 tions between distant residues in the native exteins and the intein, in three-dimensional space.
18 emselves out of precursor proteins while the exteins are ligated together.
19 o the formation of new proteins in which the exteins are linked directly by a peptide bond.
20 o the formation of new proteins in which the exteins are linked directly by a peptide bond.
21 ed and the remaining two flanking sequences (exteins) are joined.
22 eir ligation junction (called local N- and C-exteins) are strongly preferred, while other sequences c
23 ols or Cys despite an ester linkage at the C-extein branch point, and (d) an absolute requirement for
24 ctrostatic interactions between the N- and C-exteins but is reduced by elevated temperature.
25 t ligation of the flanking polypeptides, the exteins, by a peptide bond.
26 g of the flanking polypeptide sequences, the exteins, by a peptide bond.
27  of the flanking sequences, the extein-N and extein-C parts, thereby reconstituting the host protein.
28 -splicing junction in both N- and C-terminal exteins can accelerate the N-terminal cleavage rate by >
29 al residues immediately flanking the intein (exteins) can reduce the splicing rate, thereby limiting
30 netic analysis of the relationship between C-extein composition and split intein activity.
31 e their excision from flanking polypeptides (exteins) concomitant with extein ligation to produce a m
32  own excision from flanking polypeptides, or exteins, concomitant with extein ligation.
33  the intein, from flanking polypeptides, the exteins, concomitant with the specific ligation of the e
34 stoc punctiforme Npu DnaE intein after the C-extein cysteine nucleophile (Cys+1) was mutated to serin
35 used naturally split inteins suffer from an "extein dependence," whereby residues surrounding the spl
36 es ultrafast DnaE split inteins with minimal extein dependence.
37 hlights common principles that contribute to extein dependence.
38 stidine residue (His(78)) contribute to this extein dependence.
39         The C31 integrase was split into two extein domains, and intein sequences (Npu DnaEN and Ssp
40           The existence and the magnitude of extein effects require consideration for maximizing the
41 rsor proteins while ligating the surrounding extein fragments with a native peptide bond.
42  that inteins may act as switches to control extein function.
43 in splicing precursor, corresponding to an N-extein fusion of the Mxe GyrA intein.
44  identity of the C-terminal residue of the N-extein has less influence on the cleavage reaction than
45  inteins present in the same location within extein homologs from different organisms are very closel
46            Surprisingly, Mtb produced free N-extein in some conditions, and ectopic expression of Mtb
47  for the (-1) scissile peptide bond at the N-extein-intein junction was found to be approximately 12
48 n the intein and the split-host protein, the exteins, is largely unknown.
49 m is often complicated by the requirement of extein junction sequences.
50 ins, from flanking polypeptide sequences, or exteins, leading to the formation of new proteins in whi
51            Applying this assay to randomized extein libraries, we show that the nature of the extein
52 s and reactive nitrogen species inhibit SufB extein ligation by forcing either precursor accumulation
53 king polypeptides (exteins) concomitant with extein ligation to produce a mature host protein.
54 ion of defined regions of a protein prior to extein ligation, generating partially labeled proteins f
55 g polypeptides, or exteins, concomitant with extein ligation.
56                                          The exteins might thereby serve as an environmental sensor,
57 tant ligation of the flanking sequences, the extein-N and extein-C parts, thereby reconstituting the
58         In this non-canonical pathway, the C-extein nucleophile attacks a peptide bond at the N-termi
59  the intein for full activity, as can remote extein point mutations.
60 ein is compatible with any amino acid in the extein position adjacent to the N-terminal splice juncti
61 -extein specificity and only two important C-extein positions.
62 hen FKBP and FRB occupied one or both of the extein positions.
63 ld binds to two inactive split intein/enzyme extein protein fragments leading to intein fragment comp
64  that were as fast or faster than the native extein, refuting past assumptions that the naturally sel
65 udy, we investigated the roles of the last N-extein residue (-1 residue) and the intein penultimate r
66 lar insight into previous claims that the +1 extein residue affects intein catalysis.
67  a proton transfer from the first C-terminal extein residue to a conserved aspartate, which synchroni
68 tic residues are constrained by the second C-extein residue, likely forcing them into an active confo
69 riplet (WCT) and a Thr or Ser as the first C-extein residue.
70 niprecursor (VMA29) containing 10 N-terminal extein residues and 4 C-terminal extein residues.
71 the Ssp DnaE intein containing five native N-extein residues and maltose binding protein as the N-ext
72 conditions and also in the absence of native extein residues flanking the intein.
73  N-terminal extein residues and 4 C-terminal extein residues.
74 ue with alanine and mutation of the native C-extein residues.
75 TS activity in the presence of unfavorable N-extein residues.
76 dependence on the sequence of its N-terminal extein residues.
77 ing a hexahistidine sequence as the N- and C-exteins, respectively.
78 y sequence similarity to only the selected C-extein sequence.
79 y may be affected by both the intein and the extein sequence.
80 mptions that the naturally selected flanking extein sequences are optimal for splicing.
81 with concomitant linkage of the two flanking extein sequences by a native peptide bond.
82                                          The extein sequences immediately flanking the intein affect
83 ution of the split intein, were fused to the extein sequences of the split intein halves.
84 ith the concomitant ligation of the flanking extein sequences to yield a new polypeptide.
85                           The novel selected extein sequences were sufficient to promote splicing in
86  In this study, genetic selection identified extein sequences with Ser+1 that enabled the Npu DnaE in
87  together with the ligation of the flanking "extein" sequences.
88 ences than previously thought, with little N-extein specificity and only two important C-extein posit
89 in libraries, we show that the nature of the extein substrate bordering the intein can profoundly inf
90 ysis showed splicing rates with the selected exteins that were as fast or faster than the native exte
91 sion from flanking polypeptide sequences, or exteins, thereby leading to the formation of new protein
92 eins and ligate their flanking polypeptides (exteins) through a multistep chemical reaction.
93                                 The enhanced extein tolerance of Cat* reported here should expand the
94 t 100 amino acids each, fused to appropriate exteins, was recently derived from the Mycobacterium tub
95 ltose-binding protein (MBP) and a His-tag as exteins were expressed from a constitutive promoter afte
96  the intein, from flanking polypeptides, the exteins, which are concomitantly joined by a peptide bon
97  This partnership between the intein and its exteins, which implies coevolution of the parasitic inte
98 rikoshii is strongly regulated by the native exteins, which lock the intein in an inactive state.
99 esidues and maltose binding protein as the N-extein with the C-terminal Ssp DnaE intein splicing doma
100  concatenation of the flanking polypeptides (exteins) with a native peptide bond.