ライフサイエンスコーパス: CTD

1 CTD also alters lipid homeostasis, cell wall integrity,

2 CTD also perturbed endoplasmic reticulum (ER) homeostasi

3 CTD suppresses tumor growth by inducing apoptosis, cell

4 CTD Tyr1-phosphorylated RNAPII (CTD Y1P) synthetizes str

5 4 independently regulates CDK9/phospho-Ser 2 CTD RNA Pol II recruitment to the IRF3-dependent IFN-sti

6 e Pediatric Cardiac Genomics Consortium: 355 CTD trios and 192 LVOTD trios.

7 ct defect (LVOTD) case-parent trios, and 406 CTD cases (n=406) and 2976 pediatric controls.

8 he prion-like C-terminal fragments of TDP-43 CTD (TDP-43 C-terminal domain), formed upon proteolytic

9 ract with and differentially modulate TDP-43 CTD aggregation and/or liquid-liquid phase separation in

10 promoted insoluble aggregates of the TDP-43 CTD while GRN-5 mediated liquid-liquid phase separation.

11 N-3 and GRN-5 could interact with the TDP-43 CTD.

12 ishes the highly similar pSer(2) and pSer(5) CTDs.

13 A CTD interaction domain (CID) from the protein Nrd1 can p

14 A CTD-dependent genetic interaction profile of CRG1 reveal

15 otomer interface is unique and consists of a CTD coiled around a beta-sheet which makes contacts with

16 ats supports Drosophila viability but that a CTD with enough YSPTSPS repeats to match the length of t

17 catalytic site, consisting of NTD loop-1 and CTD loop-3.

18 K12 inhibition on transcription activity and CTD phosphorylation in human cells.

19 ntly from reconfiguration of the NTD-CTD and CTD trimer interfaces.

20 PF subunits Ppn1, Swd22, Ssu72, and Ctf1 and CTD mutation T4A.

21 the interactions between deoxy-cytidines and CTD loop-1 and loop-7 residues were different from those

22 The CTD dimer and CTD trimer interfaces are also intrinsically variable.

23 an absence of cross talk between the NTD and CTD during conformational changes of the S protein.

24 rminal and C-terminal domains of CA (NTD and CTD, respectively) engage in both homotypic and heteroty

25 The NED, NTD, and CTD of the outer monomers are disordered in intasome str

26 In contrast, DYRK1A, another CTD kinase known to control transcription of a subset of

27 al domain of the bacteriophage phi29 ATPase (CTD) that suggest a structural basis for these functiona

28 ients, those randomly assigned to attenuated CTD (CTDa) induction had a higher risk of VTE compared w

29 only the J and C-terminal substrate binding (CTD) domains but also the functionally important linkers

30 which interferes with E2 binding to the Brd4 CTD, and that this interaction is required for initiatio

31 ) (pSer(5)) is gradually dephosphorylated by CTD phosphatases, whereas Ser(2) phosphorylation accumul

32 CA NTD can functionally replace the HIV-1 CA CTD, but the HIV-1 CA NTD cannot replace the HTLV-1 CA C

33 he HIV-1 CA NTD cannot replace the HTLV-1 CA CTD, indicating that the HTLV-1 CA subdomains provide di

34 7-amino-acid sequence, called the canonical CTD, which orchestrates various steps in mRNA synthesis.

35 Cantharidin (CTD) is a potent anticancer small molecule produced by s

36 TDs, and inactivation of Crkl in mice causes CTDs, thus implicating this gene as a modifier.

37 s provide the first direct evidence that CDF CTDs play a role in metal selectivity.

38 Chlorthalidone (CTD) is more potent than hydrochlorothiazide (HCTZ) in r

39 ct experimental evidence for a combinatorial CTD phosphorylation code wherein previously installed mo

40 ts, the LVOTD cohorts, and from the combined CTD and LVOTD cohorts.

41 Moreover, mutation of the conserved CTD SUMOylation sites perturbs Aurora B recruitment and

42 N-terminal domain (NTD) with eIF4A, and Ded1-CTD with eIF4G, subunits of eIF4F, enhance Ded1 unwindin

43 4A/eIF4E unveiled a requirement for the Ded1-CTD for robust initiation.

44 Philadelphia: 670 conotruncal heart defect (CTD) case-parent trios, 317 left ventricular obstructive

45 Creatine Transporter Deficiency (CTD) is an inborn error of metabolism presenting with in

46 phosphamide, thalidomide, and dexamethasone (CTD) (22.5% [n = 121 of 538] vs 16.1% [n = 89 of 554]; a

47 DS) is a systemic connective tissue disease (CTD) associated with a predisposition for intestinal inf

48 ith idiopathic or connective tissue disease (CTD)-related ILD and 13 controls.

49 rette syndrome (TS) or chronic tic disorder (CTD) have an elevated risk of subsequent substance misus

50 ith pin1Delta, a Y1F mutant does not, nor do CTD mutants in which half the Pro3 or Pro6 residues are

51 gate domain, and a large cytoplasmic domain (CTD) that contains the Ca(2+) sensors.

52 domain (NTD) and a C- terminal motor domain (CTD).

53 in (NTD) and a C-terminal regulatory domain (CTD); a carotenoid spans the two domains.

54 sphorylated RNAPII C-terminal repeat domain (CTD) phosphorylated on both Ser2 and Ser5 and are detect

55 ive, weakly ssDNA binding C-terminal domain (CTD) and a catalytically inactive, strongly ssDNA bindin

56 rine-2 (S2) in the RNAPII C-terminal domain (CTD) and promotes transcript elongation.

57 cations on the RNA pol II C-terminal domain (CTD) and the chromatin template.

58 tion patterns of the Rpb1 C-terminal domain (CTD) and the factors that recognize them change as a fun

59 le of the channel-and the C-terminal domain (CTD) as well as hydrophobic interactions between the hig

60 ain (NTD) and a catalytic C-terminal domain (CTD) connected by a short linker.

61 of the RNA polymerase II C-terminal domain (CTD) coordinate the transcription cycle.

62 printing, a region in the C-terminal domain (CTD) exhibits a differential behavior, potentially highl

63 le genes related to carboxy-terminal domain (CTD) family proteins, including the gingipains, were upr

64 s in two states, with its C-terminal domain (CTD) folded either as alpha-helical hairpin or beta-barr

65 f these proteins bind the C-terminal domain (CTD) of FtsZ, which serves as a hub for FtsZ regulation.

66 established that the long C-terminal domain (CTD) of H1 remains disordered upon nucleosome binding an

67 se (MTase) domain and the C-terminal domain (CTD) of L adopt a unique conformation, positioning the M

68 hat an excess of the free C-terminal domain (CTD) of ParB impeded DNA condensation or promoted decond

69 ation, phosphorylates the C-terminal domain (CTD) of Pol II and negative elongation factors to releas

70 ted the importance of the C-terminal domain (CTD) of Pol IV's largest subunit given that the Pol II C

71 elongation factor binding C-terminal domain (CTD) of ribosomal P stalk proteins to inhibit translatio

72 phosphorylates the carboxyl-terminal domain (CTD) of RNA polymerase II (pol II) but its roles in tran

73 The C-terminal domain (CTD) of RNA polymerase II (Pol II) is composed of repeat

74 the phosphorylated carboxy-terminal domain (CTD) of RNA polymerase II (RNAPII) using RGG motifs in i

75 on by phosphorylating the C-terminal domain (CTD) of RNA polymerase II (RNAPII).

76 The C-terminal domain (CTD) of RNA polymerase II contains a repetitive heptad s

77 ructurally related to the C-terminal domain (CTD) of RNA polymerase II.

78 lation of serine-2 in the C-terminal domain (CTD) of RNA-polymerase II (Pol II), and reduces the expr

79 ested the function of the C-terminal domain (CTD) of Rpf2 during these anchoring steps, by truncating

80 ER) membranes, the carboxyl-terminal domain (CTD) of SREBPs binds to the CTD of Scap.

81 ted the proposal that the C-terminal domain (CTD) of the AMPAR subunit GluA1 is required for LTP.

82 core domain (CCD) and the C-terminal domain (CTD) of the integrase.

83 ates Ser2 residues of the C-terminal domain (CTD) of the largest subunit (RPB1) of RNA polymerase II

84 Interest in the C-terminal domain (CTD) of the RPB1 subunit of the RNA polymerase II (Pol I

85 the Y320A mutation in the C-terminal domain (CTD) of the S1 subunit, indicating that there might be a

86 the putative coiled-coil C-terminal domain (CTD) of the SMARCB1 (BAF47) subunit, which cause the int

87 ent of RDCs in the mobile C-terminal domain (CTD) of the stalk protein bL12.

88 nt-specific Pol II carboxyl terminal domain (CTD) phosphatase, to form the BAH-PHD-CPL2 complex (BPC)

89 y phosphorylated at carboxy-terminal domain (CTD) residue Tyr1, at DSBs.

90 t and phospho-Ser 2 carboxy-terminal domain (CTD) RNA polymerase (Pol) II formation on the promoters

91 cial site between TMD and C-terminal domain (CTD) that modulates the Zn(2+) transport activity of HsZ

92 in the RNA polymerase II C-terminal domain (CTD) to citrulline, uncovering a potential regulatory pa

93 ith the RNA polymerase II C-terminal domain (CTD) to establish proper levels and distribution of H3K4

94 II) contains a disordered C-terminal domain (CTD) whose length enigmatically correlates with genome s

95 perphosphorylation of its C-terminal domain (CTD).

96 UMOylation of the Topo II C-terminal domain (CTD).

97 ree copies of the Redbeta C-terminal domain (CTD).

98 for association with its C-terminal domain (CTD).

99 he protein and the entire C-terminal domain (CTD).

100 a regulatory cytoplasmic C-terminal domain (CTD).

101 6b oligomerization in its C-terminal domain (CTD).

102 deleted the distal carboxyl terminus domain (CTD) of the cold-activated melastatin receptor channel,

103 repeat domains (ARD) and C-terminal domains (CTD).

104 c core (CCD), and carboxyl terminus domains (CTD).

105 s in how the Rb and p107 C-terminal domains (CTDs) associate with the coiled-coil and marked-box doma

106 DNA motifs, via diverged C-terminal domains (CTDs).

107 match the length of the wild-type Drosophila CTD is defective.

108 th each other, are both needed for efficient CTD binding in Saccharomyces cerevisiae.

109 K7ac enhanced CTD peptide binding to the CTD-interacting domain (CID)

110 from Drosophila melanogaster), an essential CTD phosphatase that dephosphorylates pSer(5) at the tra

111 Disorder is highly conserved and facilitates CTD-CTD interactions, an ability we show is separable fr

112 ith well-established behavioral readouts for CTD mice, to longitudinally study the therapeutic effica

113 ants were associated with increased risk for CTDs (odds ratio [OR) ranges: 1.64-4.75).

114 LCR22A-D region are associated with risk for CTDs on the basis of the sequence of the 22q11.2 region

115 Our new approach concluded that the free CTD blocks the formation of ParB networks by heterodimer

116 main and chelated by conserved residues from CTD and the His-Cys-His (HCH) motif from the N-terminal

117 fic length variations, and possibly fulfills CTD related functions in gene regulation.

118 ells, the functional requirement of the full CTD for the control of Pol II activity at endogenous mam

119 increases in data content and functionality, CTD has upgraded its computational infrastructure.

120 the condensation of the nucleosome-bound H1 CTD.

121 d linker histone carboxy-terminal domain (H1 CTD) influences chromatin structure and gene regulation

122 nt evidence that the H3 N-tail influences H1 CTD condensation through direct protein-protein interact

123 upport an emerging hypothesis wherein the H1 CTD serves as a nexus for signaling in the nucleosome.

124 patients with nested LCR22C-D deletions have CTDs, and inactivation of Crkl in mice causes CTDs, thus

125 In free RfaH, the alpha-helical CTD interacts with, and masks the RNA polymerase binding

126 phosphorylation to generate a heterogeneous CTD modification landscape that expands the CTD's coding

127 show that the acidic tip of the E. coli Hfq CTD transiently binds the basic Sm core residues necessa

128 Finally, we describe how the Hfq CTD and its acidic tip residues provide a mechanism to m

129 Here, we investigate how CTD length and disorder influence transcription.

130 However, CTDs with too many YSPTSPS repeats are more prone to loc

131 l IV's largest subunit given that the Pol II CTD mediates multiple aspects of Pol II transcription.

132 ase refractory to MFH290 and restored Pol II CTD phosphorylation and DNA damage repair gene expressio

133 ts both Ser2 and Ser5 residues of the pol II CTD.

134 e Thr4 phospho-site in the RNA polymerase II CTD and the 3' processing/termination factors CPF and Rh

135 function of SSU72 homolog, RNA polymerase II CTD phosphatase (Ssu72, from Drosophila melanogaster), a

136 hybrid formation or dsRNA processing impairs CTD Y1P foci formation, attenuates DART synthesis and de

137 These updates continue to improve CTD and help inform new testable hypotheses about the et

138 IIbeta function may be due to differences in CTD charge distribution and differential alignment of th

139 -repress Pho1 acid phosphatase expression in CTD-T4A cells.

140 We also report a 46% increase in CTD manually curated content, which when integrated with

141 These findings suggest that variance in CTD penetrance in the 22q11.2DS population can be explai

142 ltransferase that methylates and inactivates CTD.

143 Both full-length TDP-43 and its CTD are also known to form stress granules by coacervati

144 ons of its NTD with eIF4E and eIF4A, and its CTD with eIF4G.

145 After SREBP2 is cleaved in Golgi, its CTD remains bound to Scap and returns to the ER with Sca

146 radation signal in a different region of its CTD.

147 ermore, 33277 and 381 mutant strains lacking CTD cell surface proteins were more immune-stimulatory t

148 different metals bind distinctively to MamM CTD in terms of their binding sites, thermodynamics, and

149 hes, the binding of different metals to MamM CTD was characterized.

150 epresses transcription through CPL2-mediated CTD dephosphorylation, thereby causing inhibition of Pol

151 Metazoan CTDs have well-conserved lengths and sequence compositio

152 o its interaction with phospho-Ser2-modified CTD.

153 plasmid increases without the outer monomer CTDs present.

154 We designed NTD-CTD hybrid proteins, and hybrid res sites containing bot

155 redominantly from reconfiguration of the NTD-CTD and CTD trimer interfaces.

156 ues in the hexamer central pore, and the NTD-CTD linker region, are well defined.

157 The structure of Nup84-Nup133(CTD) details the high flexibility of this dimeric unit o

158 e phosphorylation states of Ser(2)/Ser(5) of CTD in RNA polymerase II that occur at different stages

159 However, details of CTD association remain unclear.

160 ssion and erases the de-repressive effect of CTD-S7A.

161 iption also evoked a hyperphosphorylation of CTD Ser2 residues at 5' ends of genes that is conserved

162 cis-trans isomerization of CTD prolines expands the scope of the code in ways that

163 Through in vitro reconstruction of CTD phosphorylation, mass spectrometry analysis, and chr

164 ription elongation and a global reduction of CTD Ser2 and Ser5 phosphorylation.

165 The role of CTD phosphorylation in virion secretion, if any, has rem

166 spective for the mechanistic significance of CTD length and disorder in transcription across eukaryot

167 ber of studies have shown that the status of CTD modifications is associated with the activity of Pol

168 n GPI-anchor remodeling is the key target of CTD, independently of PP2A and PP1 activities.

169 e identified additional molecular targets of CTD using a Saccharomyces cerevisiae strain that express

170 of three genome-wide association studies of CTDs in affected individuals without 22q11.2DS.

171 EC components dependent on CTD phosphorylation include capping enzyme, cap-binding

172 both antiviral properties of IFITM3, but one CTD mutant exhibited a divergent behavior, possibly high

173 de, lenalidomide, and dexamethasone (CRD) or CTD.

174 Instead, the outer CTDs contribute to aggregation of PFV intasomes which ma

175 Deletion of the outer CTDs enhances the lifetime of the intasome compared to f

176 tion domain (P(OD)) and C-terminal domain (P(CTD)) of a tetramer of P.

177 Deletion of P1 CTD, but not P2 CTD reduced the affinity of the pentamer

178 A crystal structure of the p107 CTD bound to E2F5 and its dimer partner DP1 reveals the

179 Deletion of P1 CTD, but not P2 CTD reduced the affinity of the pentamer for RTA.

180 Through interactions with the phosphorylated CTD and nascent RNA, hnRNPG associates co-transcriptiona

181 modification mediated by the Phosphorylated CTD Interacting Factor 1 (PCIF1), which catalyzes m6A me

182 he repetitive sequence of the phosphorylated CTD via its N-terminal CTD-interacting domain.

183 The phosphorylation pattern of Pol2 CTD Y1S2P3T4S5P6S7 repeats comprises an informational co

184 O lncRNA termination is governed by the Pol2 CTD code and is subject to metabolite control by inosito

185 rocessing/termination machinery and the Pol2 CTD code.

186 ide association analysis of BP response post CTD treatment in African Americans (AA) and European Ame

187 Furthermore, the P stalk protein CTD is flexible and adopts distinct orientations and int

188 The Redbeta CTD forms a three-helix bundle with unexpected structura

189 ent encounter complex, allowing the refolded CTD to bind ribosomal protein S10.

190 h lower rates of VTE for identical regimens (CTD, 13.2% vs 16.1%; CTDa, 10.7% vs 16.0%).

191 One of these proteins is SR-related CTD-associated factor 4 (SCAF4), which is important for

192 te for the Set1 N-terminal region to restore CTD interactions and histone methylation.

193 -terminal domain of RNA polymerase II (RNAP2-CTD) coordinates transcription, splicing, and RNA proces

194 lymerase II carboxyl terminal domain (RNAPII CTD) kinase complex (CTK complex) is known as a positive

195 s shows that CTK-1 phosphorylates the RNAPII CTD at Ser2 residues in the cat-3 ORF region during tran

196 restricts CDK7 kinase function to the RNAPII CTD, whereas other substrates (e.g., SPT5 and SF3B1) are

197 CTD Tyr1-phosphorylated RNAPII (CTD Y1P) synthetizes strand-specific, damage-responsive

198 We conclude that the nuclear RNAPII-CTD kinase CDK12 cooperates with mTORC1, and controls a

199 The selective ablation of the RPB1 CTD, post-initiation, at promoter-proximal pause-sites r

200 We demonstrate that MamM's CTD can discriminate against Mn(2+), supporting its post

201 e present the crystal structures of the Seb1 CTD- and RNA-binding modules.

202 ced exosome RNA degradation and larger Ser2p CTD-modified RNA polymerase II foci.

203 pho1 de-repression by mutation of the Ser7 CTD letter depends on IP8.

204 We find that the SMARCB1 CTD contains a basic alpha helix that binds directly to

205 ly conserved structural role for the SMARCB1 CTD that is perturbed in human disease.

206 gulated when the cis-proline-dependent Ssu72 CTD phosphatase is inactivated.

207 Furthermore, a fluorescently tagged CTD lacking the rest of Pol II dynamically enters transc

208 nd- and third-degree relatives of OCD and TD/CTD probands.

209 ccus-related conditions) and both OCD and TD/CTD.

210 ing pregnancy was associated with risk of TD/CTD in a dose-response manner but the association was no

211 dentified, 5597 of which had a registered TD/CTD diagnosis.

212 of the phosphorylated CTD via its N-terminal CTD-interacting domain.

213 and slows down its release from it and that CTD-CTD interactions enable recruitment of multiple poly

214 Altogether, we conclude that CTD induces cytotoxicity by targeting Cdc1 activity in G

215 We found that CTD specifically affects phosphatidylethanolamine (PE)-a

216 ents with human cells further suggested that CTD functions through a conserved mechanism in higher eu

217 ch recapitulate experiments and support that CTD length promotes initial polymerase recruitment to th

218 The CTD dimer and CTD trimer interfaces are also intrinsical

219 The CTD is a member of the ubiquitous Nuclear Transport Fact

220 The CTD is crucial to eukaryotic transcription, yet the func

221 The CTD of SREBP remains bound to Scap but must be eliminate

222 pon activation, the domains separate and the CTD refolds into the beta-barrel, which recruits a ribos

223 Here, we identify a new modification at the CTD, the deimination of arginine and its conversion to c

224 nd that the stability of DNA wrapping by the CTD provides one limit to DNA supercoil introduction, be

225 pon release from the elongation complex, the CTD transforms back into the autoinhibitory alpha-state,

226 ity, fluorescence binding assays confirm the CTD retains its DNA binding capabilities and fitting the

227 In contrast, the CTD in empty HBV virions (i.e., enveloped capsids with n

228 CTD modification landscape that expands the CTD's coding potential.

229 ealed that this domain, and by extension the CTD heptads and their modifications, is functionally nei

230 its DNA binding capabilities and fitting the CTD into cryoEM density of the phi29 motor shows that th

231 highlight a previously unknown role for the CTD of SREBPs in regulating SREBP activity.

232 nome-wide association study results from the CTD cohorts, the LVOTD cohorts, and from the combined CT

233 change in solute-inaccessible volume in the CTD of ~1,900 angstrom(3) This volume matches the void s

234 pe, without other notable differences in the CTD, indicating that structural changes from the mutatio

235 3G stabilizes ssDNA binding but inhibits the CTD's search function.

236 We found that a knock-in mouse lacking the CTD of GluA1 expresses normal LTP and spatial memory, as

237 nds to an 11-mer peptide (P11) mimicking the CTD of P stalk proteins with low micromolar affinity.

238 ns between the highly conserved Y2807 of the CTD and pore-lining helices are required to ensure norma

239 phosphate groups on specific residues of the CTD are critical for the fidelity and effectiveness of R

240 ol IV-dependent loci affected by loss of the CTD are primarily located in chromosome arms, similar to

241 tion factor Rhn1, and the Thr4 letter of the CTD code.

242 However, deletion of the CTD does not phenocopy clsy or shh1 mutants, consistent

243 bacteria, was used to probe the role of the CTD in metal recognition and selectivity.

244 ished, we investigated here the roles of the CTD in the post-initiation control of Pol II.

245 The NMR solution structure of the CTD indicates it is a vestigial nuclease domain that lik

246 rming a detailed molecular dissection of the CTD of SREBP2, one of three SREBP isoforms expressed in

247 propose that the sequence complexity of the CTD offsets aberrant behavior caused by excessive repeti

248 suggest that the differential impact of the CTD on topo IIalpha and topo IIbeta function may be due

249 solution NMR studies on the structure of the CTD showed that a serine/threonine-rich stretch causes a

250 ignificant association (FDR p < 0.05) of the CTD subset with 62 common variants in a single linkage d

251 Deletion of the last 36 amino acids of the CTD transforms TRPM8 into a reduced temperature-sensitiv

252 ome, and we also found that alignment of the CTD was almost independent of the presence of the core r

253 The crystal structure of the CTD with proline mutation L390P showed a flattening of t

254 stribution and differential alignment of the CTD with reference to transport DNA.

255 These results suggest a dual role of the CTD, first in binding to lambda Exo to facilitate loadin

256 ating by stabilizing the folded state of the CTD.

257 llinates R1810 (Cit1810) at repeat 31 of the CTD.

258 gating is proportional to the length of the CTD.

259 adening, and exchange-induced shifts) on the CTD of both wild type and a point mutant (T142A) within

260 esidues, in an interaction that requires the CTD.

261 Detailed NMR analysis shows that the CTD (but not the J domain) self-associates to form an ol

262 EM density of the phi29 motor shows that the CTD directly binds DNA.

263 nscription compartments, indicating that the CTD functions as a signal sequence.

264 We show that the CTD is dispensable for Pol IV catalytic activity and Pol

265 We previously demonstrated that the CTD of H1.0 undergoes a significant condensation (reduct

266 The structure reveals that the CTD of neighboring hexamers pack in crystal contacts, an

267 e NTD was rotated 90 degrees relative to the CTD along the major axis of the molecule, an orientation

268 positively charged channel connected to the CTD catalytic site, consisting of NTD loop-1 and CTD loo

269 Stx2a holotoxin also binds to the CTD of P stalk proteins because the ribosome-binding sit

270 When bound to the CTD of Scap, this signal is masked and SREBP2 is stabili

271 terminal domain (CTD) of SREBPs binds to the CTD of Scap.

272 of a new family of proteins, homologs to the CTD, the C-terminal domain-like carotenoid proteins (CCP

273 K7ac enhanced CTD peptide binding to the CTD-interacting domain (CID) of RPRD1A and RPRD1B protei

274 r, 24 nt siRNA levels decrease ~80% when the CTD is deleted.

275 e cytoplasm, and it is not known whether the CTD takes an active regulatory role in metal recognition

276 This strongly supports a model in which the CTD acts as a key bridging interface between distal DNA

277 While the CTD catalyzes cytosine deamination, the NTD is believed

278 urely binds ssDNA through the NTD, while the CTD samples and potentially deaminates the substrate.

279 py clsy or shh1 mutants, consistent with the CTD affecting post-recruitment aspects of Pol IV activit

280 the alphaB helices located at the top of the CTDs.

281 yrA subunit of Escherichia coli gyrase (the 'CTD').

282 ferentially regulate pocket proteins through CTD phosphorylation.

283 cise array of heptad motifs, as important to CTD function.

284 antly associated with better DBP response to CTD (p = 5.76 x 10(-6), beta = -15.75) in the AA cohort.

285 o the variability observed in BP response to CTD.

286 For M. smegmatis TopoI-CTD, a 27-amino-acid tail that is rich in basic residues

287 On the contrary, we show that a truncated CTD composed solely of YSPTSPS repeats supports Drosophi

288 TS/CTD was associated with an increased risk of any subsequ

289 TS/CTD were associated with various types of subsequent sub

290 4,277,199 individuals, of whom 7832 had a TS/CTD diagnosis (76.3% men).

291 the association between ICD diagnoses of TS/CTD and substance misuse outcomes, accounting for psychi

292 tance misuse outcomes in individuals with TS/CTD was substantially attenuated but remained significan

293 nd asp1-493(Stop)-were lethal in a wild-type CTD background, they were viable in combination with mut

294 art disease, mostly of the conotruncal type (CTD), whereas others have normal cardiac anatomy.

295 r patients with LDS despite their underlying CTD.

296 In this way, CTD-Cit1810 favors RNAP2 pause release and efficient tra

297 Weakening CTD-DNA interactions slows supercoiling, impairs DNA-dep

298 Whereas CTD S2A, T4A, and S7A mutants thrive in combination with

299 et CRKL and is significantly associated with CTD risk (GH22J020946, sequence kernal association test

300 also been observed in in some patients with CTD, potentially increasing the risk of surgical interve