ライフサイエンスコーパス: kiss

1 ng teleregulation and interchromosomal "gene kissing".

2 that mediate positive regulation of GnRH by Kiss.

3 ght in adult humans, as tested in the act of kissing.

4 sites located on chromosome 1 by chromosome kissing.

5 ous mononucleosis is most likely acquired by kissing.

6 sm of regulation of Fob1-mediated chromosome kissing.

7 rous tissue results in rescued expression of KiSS-1 and reduced metastatic phenotype.

8 Sp1 are strong transcriptional regulators of KiSS-1 and that loss or decreased expression of AP-2alph

9 for the loss of tumor metastasis suppressor KiSS-1 expression and thus increased cancer metastasis.

10 Here we show that the loss of KiSS-1 expression in highly metastatic breast cancer cel

11 human chromosome 6q16.3-q23 is essential for KiSS-1 expression in normal tissues.

12 Furthermore, we demonstrate that KiSS-1 expression is regulated by Sp1 elements within th

13 ression of Sp1 and DRIP-130 not only rescues KiSS-1 expression, but also induces an inhibition of the

14 RIP-130-modulated transcriptional control of KiSS-1 expression.

15 The product of the KiSS-1 gene is absent or expressed at low level in metas

16 Loss of the metastasis suppressor gene, KiSS-1 has been strongly correlated to the progression o

17 y activate the transcriptional regulation of KiSS-1 in breast cancer cells.

18 The mechanism through which KiSS-1 is lost during metastasis, however, is still not

19 noma cells, similar to the overexpression of KiSS-1 metastasis suppressor gene in those cells.

20 The expression of KiSS-1 or KiSS1, like other tumor suppressor, is commonl

21 A polypeptide derived from the KiSS-1 product, designated kisspeptin-10 (Kp-10), activa

22 an chromosome 6q16.3-q23, results in reduced KiSS-1 promoter activation in highly malignant melanoma

23 domain, AP-2B, together with Sp1, increased KiSS-1 promoter activity dramatically, suggesting that A

24 ements within the first 100-bp region of the KiSS-1 promoter and that targeted deletion of a single G

25 y metastatic breast cell lines did not alter KiSS-1 promoter-driven luciferase gene activity.

26 ption does not require direct binding to the KiSS-1 promoter.

27 suggest that DRIP-130 is a key regulator in KiSS-1 transactivation in normal tissue, and that the lo

28 lly, suggesting that AP-2alpha regulation of KiSS-1 transcription does not require direct binding to

29 p1-binding sites of the promoter to activate KiSS-1 transcription.

30 Genes affected by WNT5A include KISS-1, a metastasis suppressor, and CD44, involved in t

31 Metastin, also known as KiSS-1, the cognate ligand for the metastin receptor GPR

32 ceptor coupled to Galphaq subunits (GPR54 or KiSS-1R).

33 e, we define genetic mechanisms that mediate Kiss action on target gene expression.

34 ese data suggest the presence of a selective kiss and run mechanism of insulin release.

35 Transient "kiss and run" interactions between endosomes containing

36 frequent cycles of fusion and fission in a 'kiss and run' pattern.

37 hormones are released through a transient ('kiss and run') or an irreversibly dilating pore (full fu

38 , mutually engaging with facial expressions, kisses and greetings.

39 nnealing can initiate through both loop-loop kissing and a distinct "zipper" pathway involving nuclea

40 a significant male bias in the initiation of kissing and a significant bias in head-turning to the ri

41 d its phosphorylation antagonized chromosome kissing and recombination and enhanced the RLS.

42 d structural changes, such as dimerization, "kiss", and cyclization.

43 or the first time that Otx-2 is regulated by Kiss, and plays a role in mediating the transcriptional

44 Visually guided eating, biting and kissing, and avoiding objects moving toward the face and

45 kiss initiators and kiss recipients for lip kissing, and took into consideration differences due to

46 Kiss-and-coat exocytosis entails prolonged maintenance o

47 ence for a third form of exocytosis, dubbed "kiss-and-coat," which is characteristic of a broad varie

48 The rapid kiss-and-hop interaction explains why tau, although bind

49 Our data imply a novel kiss-and-hop mechanism by which tau promotes neuronal mi

50 t a new membrane feature resulting from the "kiss-and-merge" granule fusion.

51 Kiss-and-run (KR) is an unconventional fusion between se

52 Kiss-and-run and reuse could enable hippocampal nerve te

53 k single vesicles through multiple rounds of kiss-and-run and reuse, without perturbing vesicle cycli

54 The increased incidence of kiss-and-run at lower frequencies may ensure that vesicl

55 The only genetic evidence for kiss-and-run at the synapse comes from mutations in the

56 meter, Qdots will not escape vesicles during kiss-and-run but only with full collapse fusion.

57 pocampal synapses and that the prevalence of kiss-and-run can be modulated by stimulus frequency.

58 Kiss-and-run dominated at the beginning of stimulus trai

59 The importance of kiss-and-run during efficient neurotransmission has rema

60 forms of compensatory endocytosis, including kiss-and-run endocytosis and a mechanism for efficient r

61 sed including clathrin-mediated endocytosis, kiss-and-run endocytosis, cavicapture, and bulk endocyto

62 his form of recycling is not compatible with kiss-and-run endocytosis; moreover, it is 200-fold faste

63 ion of openings that close without dilating (kiss-and-run events) enabled us to resolve exocytosis in

64 y synaptic vesicle endocytosis including any kiss-and-run events.

65 radox is explained by a fourfold increase in kiss-and-run exocytosis (as determined by single-granule

66 he upregulation of STXBP6 and an increase in kiss-and-run exocytosis at the expense of full fusion.

67 synaptotagmin isoform activated, and because kiss-and-run exocytosis can filter small molecules throu

68 ely slow rate of release of glutamate during kiss-and-run exocytosis shifts the population of AMPA re

69 ion pores and survive intact for future use (kiss-and-run exocytosis).

70 f a fusing vesicle are fates associated with kiss-and-run exocytosis, and we find that these are the

71 An intact cortex favors kiss-and-run exocytosis, whereas disrupting the cortex f

72 dent partial emptying of DCVs, suggestive of kiss-and-run exocytosis.

73 ) in Dictyostelium is carried out by a giant kiss-and-run focal exocytic event during which the two m

74 uminescence change allowed us to distinguish kiss-and-run from full-collapse fusion and to track sing

75 selectively release catecholamines through a kiss-and-run fusion event.

76 l cortex plays a key role in stabilizing the kiss-and-run fusion event.

77 Kiss-and-run fusion events were concentrated near the ce

78 Further work is needed to determine whether kiss-and-run is a major mode of fusion and has a major r

79 Kiss-and-run is a mode of membrane fusion and retrieval

80 echnique to provide compelling evidence that kiss-and-run is the dominant mode of vesicle fusion at h

81 thin the readily releasable pool (RRP) via a kiss-and-run mechanism that involves rapid opening and c

82 Basal sympathetic firing elicits a transient kiss-and-run mode of exocytosis and modest catecholamine

83 pore dilation and maintains the granule in a kiss-and-run mode of exocytosis.

84 cles, with long-dwelling vesicles preferring kiss-and-run rather than full-collapse fusion.

85 , including bulk retrieval and the so-called kiss-and-run recycling.

86 rom the reserve pool, placing constraints on kiss-and-run recycling.

87 However, the existence of kiss-and-run remains highly controversial, as revealed b

88 parison with FM dye destaining revealed that kiss-and-run strongly prevailed over full-collapse fusio

89 otein receptor (SNARE) complex that promotes kiss-and-run vesicle fusion.

90 Quickening of kiss-and-run vesicle reuse was also observed at higher f

91 pore, the activation of isoforms that favor kiss-and-run will select smaller molecules over larger m

92 Nonclassical fusion retrieval by kiss-and-run would be kinetically advantageous but remai

93 vents associated with "full fusion" events, "kiss-and-run" and "kiss-and-stay" exocytosis, confirming

94 By extension, clathrin-independent "kiss-and-run" endocytosis does not sustain synaptic tran

95 "Kiss-and-run" events and tubule connections mediate tran

96 me and revealed to precisely mark organelle "kiss-and-run" events.

97 In contrast, a nonclassical mode known as "kiss-and-run" features fusion by a transient fusion pore

98 onclusions dispute previous assertions that "kiss-and-run" is a major mechanism of vesicle recycling

99 The extent to which a "kiss-and-run" mode of endocytosis contributes to synapti

100 they released their contents, indicating a "kiss-and-run" pathway.

101 Transient fusion ("kiss-and-run") is accepted as a mode of transmitter rele

102 id opening and closing of a fusion pore (or "kiss-and-run") with a median opening time of 2.6 s, whic

103 ely 1 s by the reversal of fusion pores via 'kiss-and-run' endocytosis.

104 ore fleeting mode of vesicle fusion, termed 'kiss-and-run' exocytosis or 'flicker-fusion', indicates

105 tsynaptic consequences, such that so-called 'kiss-and-run' exocytosis results in negligible activatio

106 cle fusion, we found both full collapse and 'kiss-and-run' fusion at calyx-type synapses.

107 These results show that 'kiss-and-run' fusion occurs at synapses and that it can

108 ' remains controversial, and the ability of 'kiss-and-run' fusion to generate rapid synaptic currents

109 'Kiss-and-run' fusion was seen as a brief capacitance fli

110 es completely, or close rapidly to generate 'kiss-and-run' fusion.

111 t evidence argues against the occurrence of 'kiss-and-run' in hippocampal synapses.

112 es, the size of the fusion pore is unclear, 'kiss-and-run' remains controversial, and the ability of

113 Such 'kiss-and-run' vesicle fusion can in principle result in

114 cargo discharge and reducing pore closure ('kiss-and-run').

115 cycled by a second, faster mechanism called 'kiss-and-run', which operates in 1 s or less to retrieve

116 tion of flickering and closing fusion pores (kiss-and-run) is very well explained by the observed beh

117 ucture (Omega-profile), followed by closure (kiss-and-run) or merging of the Omega-profile into the p

118 Alternatively, the pore may close (kiss-and-run), but the triggering mechanisms and its end

119 ivities, their preference for full fusion or kiss-and-run, and their sensitivity to inhibition by syn

120 action of fusion events has been shown to be kiss-and-run, as determined using cell-attached capacita

121 ne invagination and vesicle reformation; (b) kiss-and-run, in which the fusion pore opens and closes;

122 as that proposed to support the presence of kiss-and-run, is likely explained by the stochastic natu

123 During kiss-and-run, syt IV increased the conductance and durat

124 retory vesicle collapses into the PM; or by "kiss-and-run," where the fusion pore does not dilate and

125 via two distinct mechanisms: full-fusion and kiss-and-run.

126 s to indicate that synaptic vesicles undergo kiss-and-run.

127 sis was shifted from full-collapse fusion to kiss-and-run.

128 n pathway via alternative mechanisms such as kiss-and-run.

129 th "full fusion" events, "kiss-and-run" and "kiss-and-stay" exocytosis, confirming that the device ha

130 regulation of postsynaptic signaling and a 'kiss-and-wait' mode of regulated membrane protein insert

131 Oral sex and open-mouthed kissing are associated with the development of oral HPV

132 ndant in thalamo-recipient cortical layers ("kissing" astrocytes), overlap markedly less.

133 (culotte or crush techniques) with mandatory kissing balloon dilatation.

134 ain vessel was stented, followed by optional kissing balloon dilatation/T-stent.

135 l success (provisional 97%, culotte 94%) and kissing balloon inflation (provisional 95%, culotte 98%)

136 cases were completed successfully with final kissing balloon inflations.

137 simple group (n=250), 66 patients (26%) had kissing balloons in addition to main-vessel stenting, an

138 ller than that of Lai, suggesting that fewer kissing base pairs are broken at the transition state of

139 Protein-mediated "chromosome kissing" between two DNA sites in trans (or in cis) is k

140 scapularis), body louse (Pediculus humanus), kissing bug (Rhodnius prolixus) and tsetse fly (Glossina

141 l and South America, Rhodnius prolixus, the "kissing bug".

142 A heat exchange mechanism in the head of kissing bugs helps to prevent stress and regulate their

143 We used thermography to examine how kissing-bugs Rhodnius prolixus actively protect themselv

144 ree steps with two obligatory intermediates (kissing complex and bent intermediate) and driven by Mg(

145 proach (referred to as enzyme-linked aptamer kissing complex assay (ELAKCA)) relied on the kissing co

146 g 2+ greatly slows down the unfolding of the kissing complex but has moderate effects on the formatio

147 We also show that loop-loop kissing complex formation becomes more efficient at phys

148 An RNA kissing complex formed by the dimerization initiation si

149 trong mechanical stability of even a minimal kissing complex indicates the importance of such loop-lo

150 nsistent with observations that the Lai-type kissing complex is more stable and requires significantl

151 , FMRP binds intramolecular G-quadruplex and kissing complex RNA (kcRNA) ligands via the RGG box and

152 Furthermore, formation of the kissing complex was dominated by base pairing, whereas i

153 igated the mechanical unfolding of a minimal kissing complex with only two G.C base pairs.

154 nt role in genome dimerization by forming a 'kissing complex' between two complementary hairpins.

155 issing complex assay (ELAKCA)) relied on the kissing complex-based recognition of the target-bound ha

156 a complex tertiary structure termed the FMRP kissing complex.

157 r nucleation through the hairpin loops in a "kissing" complex.

158 The kinetics and thermodynamics of kissing-complex formation and their subsequent strand-di

159 ns with larger loops rapidly form long-lived kissed complexes.

160 obe the factors that govern the stability of kissing complexes and their subsequent structural rearra

161 g of RNA duplex formation can be extended to kissing complexes but that kissing complexes display an

162 In some cases, kissing complexes can be a prelude to strand displacemen

163 Formation and stability of these RNA kissing complexes depend crucially on cationic condition

164 an be extended to kissing complexes but that kissing complexes display an unusual level of stability

165 In minimal RNA kissing complexes formed between hairpins with cognate G

166 The two kissing complexes have distinct unfolding transition sta

167 primary difference between stable and labile kissing complexes is based almost completely on their of

168 ither Mal-type (GUGCAC) or Lai-type (GCGCGC) kissing complexes under various ionic conditions.

169 tion and dissociation dynamics of individual kissing complexes, as well as the formation of the matur

170 sites that are complementary partners of a "kissing" contact across the dimer interface.

171 timulates refolding of SL1 from a metastable kissing dimer (KD) into thermodynamically stable linear

172 nce in its apical loop, forming a metastable kissing dimer form.

173 First, a metastable kissing dimer is formed via a loop-loop interaction and

174 First, a metastable kissing dimer is formed via standard Watson-Crick base p

175 iciency virus type I that forms a metastable kissing dimer that is converted during viral maturation

176 ich facilitates the in vitro conversion from kissing dimer to extended dimer.

177 Our studies indicate that a kissing dimer-mediated structure, if formed, exists only

178 ization mass spectrometry was used to detect kissing dimers in a multiequilibria mixture, whereas opt

179 ly conserved internal loop that promotes the kissing-duplex transition by a mechanism that remains po

180 ing, Mg2+ may increase the dependence of the kissing-duplex transition on NC binding thus preventing

181 loop in an SL1 monomer that may promote the kissing-duplex transition.

182 putative expression of estrogen receptors in kiss-expressing cells and, finally, we investigated whet

183 Most teleosts have two kiss genes, kiss1 and kiss2, but their sites of expressi

184 signal (DIS) that has been proposed to form kissing hairpin and/or extended duplex intermolecular co

185 Kissing hairpin interactions form when the loop residues

186 follows: the loop-loop interactions found in kissing hairpins or the stem-stem interactions of a cruc

187 Kisspeptins (Kiss) have been shown to be key components in the regula

188 We investigated head-turning bias in both kiss initiators and kiss recipients for lip kissing, and

189 nt bias in head-turning to the right in both kiss initiators and kiss recipients, with a tendency amo

190 dimerization is initiated through an RNA-RNA kissing interaction formed via the dimerization initiati

191 intramolecular kissing interaction, and the kissing interaction forms only after the folding of the

192 e distribution, the kinetics of breaking the kissing interaction is calculated as a function of force

193 The force required to disrupt the kissing interaction of the two structures, the rip force

194 This loop has been implicated in a kissing interaction with a complementary stem-loop struc

195 A structure is kinetically stabilized by the kissing interaction, and extra work is required to unfol

196 nfold only after breaking the intramolecular kissing interaction, and the kissing interaction forms o

197 interacts with the CRE in the absence of the kissing interaction.

198 ucleosides and examined their effects on the kissing interaction.

199 hairpins participate in intermolecular cross-kissing interactions (SL-C to SL-D' and SLC' to SL-D) an

200 In a unimolecular context, kissing interactions are important for tertiary folding

201 the cellular environment and that loop-loop kissing interactions involving Stem 3 modulate -1 PRF an

202 s and that 5BSL3.2 engages simultaneously in kissing interactions using its apical and internal loops

203 t allows us to treat a variety of miRNA-mRNA kissing interactions, which have been ignored in the cur

204 t, in isolated RNAs, are capable of forming "kissing" interactions stabilized by two intermolecular G

205 Oligomerization of Fob1 caused synaptic (kissing) interactions between pairs of terminator (Ter)

206 allow, and blow normally whereas pouting and kissing is still difficult.

207 iss1 gene and a single Kiss1r gene, multiple Kiss ligand and receptor genes are found in nonmammalian

208 t allows RNA dimerization via intermolecular kissing loop (KL) base pairing.

209 ribozyme core via three tertiary contacts: a kissing loop (P14), a metal core-receptor interaction, a

210 structure assembled from common elements, a kissing loop and two three-way junctions.

211 ormation of an extended duplex rather than a kissing loop complex because the short stems are not sta

212 The degree of cation accumulation around the kissing loop complex was also inversely proportional to

213 two other RNAs, an adenine riboswitch and a kissing loop complex, become more stable by 2-3 kcal/mol

214 m-loop interface to allow the formation of a kissing loop complex.

215 op interface is critical in the formation of kissing loop complexes and that in the absence of Mg(2+)

216 Kissing loop complexes are loop-loop complexes where two

217 Our results show that although kissing loop complexes form more readily in the presence

218 rived from the ColE1 plasmid to associate as kissing loop complexes in the presence and absence of di

219 Readily reversible kissing loop formation combined with slow cleavage of th

220 However, we showed that kissing loop formation improves ligand binding efficienc

221 An RNA kissing loop from the Moloney murine leukemia virus (MML

222 Recognition of the substrate involves a kissing loop interaction between the substrate and the c

223 To analyze the role of the kissing loop interaction in the riboswitch regulatory me

224 We found that the kissing loop interaction is not essential for ligand bin

225 Escherichia coli btuB riboswitch contains a kissing loop interaction that is in close proximity to t

226 A kissing loop is a highly stable complex formed by loop-l

227 ubstrate stem loop I (SLI)-stem loop V (SLV) kissing loop junction of the Varkud Satellite ribozyme h

228 to analyze the binding and dynamics of this kissing loop junction.

229 ranscriptional expression possibly through a kissing loop model bridging TRX 3'- and 5'-UTRs through

230 he basis of the palindromic nature of SL1, a kissing loop model has been proposed.

231 indromic nature of the apical loop of SL1, a kissing loop model has been proposed.

232 ection pathway resembles that of an isolated kissing loop similar to P14, and the rate along the indu

233 alter the observed counterion specificity in kissing loop stability.

234 These oligomers self-associate to form a kissing loop that thermally rearranges into a more stabl

235 ed metastable configuration consisting of a "kissing loop" stabilized by flanking helical domains; th

236 In contrast, a 'kissing loop' interaction between the terminal loop of S

237 The presence of the 'kissing loop' interaction inhibited the formation of SL9

238 By monitoring the folding of the aptamer, kissing loop, and riboswitch expression platform, we est

239 n that the Tar-Tar(*) complex, an archetypal kissing loop, can form without Mg(2+), so long as high c

240 ion of the MMLV dimerization initiation site kissing loop.

241 involves the fast formation of an unstable "kissing" loop intermediate, followed by a slower convers

242 the fast formation of an unstable extended "kissing" loop intermediate, followed by a slower strand

243 d that SARS-CoV RNA dimers assemble through 'kissing' loop-loop interactions.

244 nucleocapsid (NC) to the hinge region of the kissing-loop (KL) dimer formed by stemloop 1 (SL1) can h

245 complementary sequences to form a metastable kissing-loop (KL) dimer.

246 sociated with the disruption of a long-range kissing-loop (KL) interaction is substantially decreased

247 it requires as much force to break the MMLV kissing-loop complex as is required to unfold an 11-bp R

248 in the unusual stability of other retroviral kissing-loop complexes such as the HIV dimerization site

249 we use to construct a Markov state model for kissing-loop dissociation.

250 ly as an unstructured spacer to position the kissing-loop elements.

251 Using this system, we determine that the kissing-loop interaction between 5BSL3.2 and 3' SL2 is r

252 bilizes an unusual long-range intramolecular kissing-loop interaction that controls mRNA expression.

253 o engages in a stable, long-distance RNA-RNA kissing-loop interaction with a 12-bp 5'-coding-region h

254 contains an apical loop capable of forming a kissing-loop interaction with a 5' proximal hairpin and

255 Most 3'CITEs participate in a long-distance kissing-loop interaction with a 5' proximal hairpin to d

256 the PEMV PTE that engages in a long-distance kissing-loop interaction with a coding sequence hairpin

257 or eIF4F complex and to engage in an RNA-RNA kissing-loop interaction with a hairpin loop located at

258 The resulting kissing-loop interaction, common in tick-borne flaviviru

259 iform is not an absolute requirement for the kissing-loop interaction, suggesting a model in which tr

260 Finally, we show that both the poly(U) and kissing-loop RNA elements can function outside of their

261 slated region (3'UTR), the ribosome-binding, kissing-loop T-shaped structure (kl-TSS) and eukaryotic

262 EMV) 3' translational enhancer, known as the kissing-loop T-shaped structure (kl-TSS), binds to 40S s

263 tifunctional element is designated a kl-TSS (kissing-loop T-shaped structure) to distinguish it from

264 B coding region, 5BSL3.2, forms a functional kissing-loop tertiary structure with part of the 3' NTR,

265 two classes of tertiary interactions, namely kissing loops and a pseudoknot.

266 The cationic uptake by kissing loops depends on the number of basepairs between

267 that were fluorescently labelled in and near kissing loops.

268 that a family of F-box proteins, called the kiss me deadly (KMD) family, targets type-B ARR proteins

269 wide kinase-interacting substrate screening (KISS) method, we identified that YopO phosphorylates a w

270 ty of both hairpin functional nucleic acids, kissing motifs, and enzyme-based signaling systems, ELAK

271 CaMP6 fiber photometry, we find that the ARN(KISS) neuron population exhibits brief ( approximately 1

272 s aimed at resetting the activity of the ARN(KISS) neuron population with halorhodopsin were found to

273 These observations indicate the ARN(KISS) neurons as the long-elusive hypothalamic pulse gen

274 The selective optogenetic activation of ARN(KISS) neurons for 1 min generated pulses of LH in freely

275 role of the arcuate nucleus kisspeptin (ARN(KISS)) neurons in LH pulse generation.

276 pi6), we show that Spi6 protects DC from the kiss of death by inhibiting granzyme B (GrB) delivered b

277 ugh contact-mediated cytotoxicity (so-called kiss of death) has proved to be controversial.

278 ignificant differences in the frequencies of kissing or sexual and relationship satisfactions.

279 mes to late endosomes followed by transient (kissing) or complete fusions between late endosomes and

280 er risk of infection than those reporting no kissing (P < .01).

281 matched odds ratio [mOR], 15.0; P = .03), >1 kissing partner (mOR, 13.66; P = .03), and attending bar

282 rtners (P = .046, for trend) or open-mouthed kissing partners (P = .023, for trend) but not vaginal s

283 These ARN(KISS) population events were found to be near-perfectly

284 oupled receptor, GPR54 (kisspeptin receptor, Kiss-R), are critical for the control of reproduction in

285 d to saporin (SAP) to selectively inactivate Kiss-R1-expressing neurons.

286 ead-turning bias in both kiss initiators and kiss recipients for lip kissing, and took into considera

287 s and kiss recipients, with a tendency among kiss recipients to match their partners' head-turning di

288 ing to the right in both kiss initiators and kiss recipients, with a tendency among kiss recipients t

289 lls and DC-HEL that are best described by a "kiss-run and engage" model, whereas control B cells had

290 Two dimerization initiation site kissing sequences, Mal and Lai, have been found in most

291 The BTE forms a kissing stem-loop interaction with the 5' UTR to mediate

292 rated an increase in GnRH gene expression by Kiss suggesting regulation of GnRH at both the secretory

293 d by Santiago Ramon y Cajal as "protoplasmic kisses that appear to constitute the final ecstasy of an

294 Saccharomyces cerevisiae promoted chromosome kissing that initiated rDNA recombination and controlled

295 ity to the mRNA 5' end of the stem-loop that kisses the 3' BTE.

296 mRNA, protein, and binding to the KsRE after Kiss treatment were demonstrated.

297 To define the mechanism of regulation, Kiss was first shown to induce nucleosome-depleted DNA w

298 Kissing was a significant risk for primary EBV infection

299 Fob1 oligomerization and Ter-Ter kissing were regulated by intramolecular inhibitory inte

300 Subjects reporting deep kissing with or without coitus had the same higher risk