ライフサイエンスコーパス: KS

1 KS also presents in individuals without HIV infection in

2 KS and NHL diagnoses during 1996 to 2011 were identified

3 KS can develop following organ transplantation through r

4 KS incidence rates among PLWH have decreased nationally

5 KS incidence rates per 100000 person-years were 52 in th

6 KS incidence was highest during the early period 4-24 mo

7 KS is a highly disseminated and vascularized tumor.

8 KS lesion cells exhibit many similarities to neuroendocr

9 KS rates among PLWH decreased significantly (average APC

10 KS risk was 5 times higher in South African women (aHR,

11 KS risk was lower in girls than in boys (adjusted HR [aH

12 KS spindle cells, the main tumor cells, all contain KSHV

13 KS tumors support both latent and lytic KSHV replication

14 KSs must recognize multiple chemically distinct ACPs and

15 Over a period of 1066572 person-years, 2046 KS cases were diagnosed.

16 ntified a GLI3 loss-of-function variant in a KS individual.

17 lidated a GLI3 loss-of-function variant in a KS individual.

18 mpound 2 for all anions investigated, with a KS/KR ratio of up to 2.

19 -throughput screen for functional hybrid ACP-KS partnerships as well as the discovery of novel antimi

20 fication of small molecule inhibitors of ACP-KS interactions.

21 tive measure of mechanistically relevant ACP-KS interactions.

22 Between 2008 and 2016, the age-adjusted KS rate among PLWH was 116/100 000.

23 There is no effective treatment for advanced KS; therefore, the survival rate is low.

24 In sub-Saharan Africa, KS continues to have a poor prognosis.

25 R gene frequencies in 250 classic (non-AIDS) KS cases, 280 KSHV-seropositive controls, and 576 KSHV-s

26 The high incidence of AIDS-KS has been ascribed to the interaction of KSHV and HIV-

27 svirus (KSHV) is etiologically linked to all KS forms, but mechanisms underlying KS development are u

28 the prevalence of AIDS-related KS, although KS does occur in individuals with well-controlled HIV in

29 In Europe, Latin, and North America KS risk was 6 times higher in men who have sex with men

30 (DEGs) overlapped between TS and female and KS and male comparisons; and these almost uniformly disp

31 6 cases of donor-derived HHV-8 infection and KS investigated from July 2018 to January 2020.

32 ANA-specific Cas9 against KSHV infection and KS.IMPORTANCE The ability for Kaposi's sarcoma-associate

33 The prevalence for both KSHV and KS are highest in sub-Saharan Africa where HIV-1 infecti

34 eir potential role in HHV-8 pathogenesis and KS.IMPORTANCE Here we show that HHV-8, a DNA tumor virus

35 ictive performance in comparison with RS and KS algorithms, in particular regarding sensitivity and s

36 /ENO2 in KSHV-infected KS tissue samples and KS visceral tissue microarrays.

37 lar mechanisms for gene regulation in TS and KS that transmit the gene dosage changes to the transcri

38 her CD4 counts and lower HIV RNA values, and KS occurred more frequently after ART initiation.

39 not pathological aggregates, but rather are KS-WNK1-dependent microdomains of the DCT cytosol that m

40 herapeutic targets to combat KSHV-associated KS.

41 igations into effector cell function between KS and asymptomatic individuals are needed to determine

42 ciated malignancy is etiologically caused by KS-associated herpesvirus (KSHV).

43 the poorest predictive response, followed by KS which showed good accuracy towards prediction, but re

44 atures governing substrate discrimination by KSs.

45 Kgamma were backcrossed into db/+ mice C57BL/KS (>10 generations) to obtain db/db-PI3Kgamma(-/-) mice

46 without HIV infection in older men (classic KS), in sub-Saharan Africa (endemic KS) and in transplan

47 have reported a higher prevalence of classic KS in diabetic patients.

48 istic support for the association of classic KS with diabetes.

49 mumax), nitrite half saturation coefficient (KS), oxygen half saturation coefficient (KO), and biomas

50 n both the discovery and validation cohorts, KS was associated with HLA-A*11:01 (adjusted OR for the

51 well as novel therapeutic targets to control KS lesions.IMPORTANCE Kaposi's sarcoma-associated herpes

52 iofacial, intellectual, and cardiac defects, KS is also characterized by humoral immune deficiency an

53 We describe a case of probable donor-derived KS in the recipient of a liver-kidney transplant.

54 uthern Africa, Europe and Asia; 26 developed KS after starting cART.

55 Four of the 6 recipients who developed KS died from KS or associated complications.

56 idence rates and risk factors for developing KS in different periods after starting cART in patients

57 idence rates and risk factors for developing KS up to 90 and 180 days and 1, 2, 5, and 8 years after

58 ther regions, have a high risk of developing KS after cART initiation.

59 not associated with the hazard of developing KS in the first year after cART initiation, but was over

60 cell counts increased the risk of developing KS throughout all observation periods after cART initiat

61 endemic KS patients suggest that KSHV drives KS pathogenesis, whereas HIV-1 exacerbates it.

62 sought to understand the mechanisms driving KS-associated immune deficiency (hypogammaglobulinemia [

63 reveal conformational states accessed during KS catalysis.

64 lutionarily conserved features in elongating KSs.

65 bearing ACPs in complex with the elongating KSs from Escherichia coli, FabF and FabB, in order to be

66 (classic KS), in sub-Saharan Africa (endemic KS) and in transplant recipients (iatrogenic KS).

67 were similar between epidemic KS and endemic KS patients (P = 0.3).

68 n reaction-confirmed epidemic KS and endemic KS patients and non-cancer controls from sub-Saharan Afr

69 okine responses between epidemic and endemic KS patients suggest that KSHV drives KS pathogenesis, wh

70 iters were higher in epidemic KS and endemic KS patients than in controls (P < .05).

71 rization of KSHV immune responses in endemic KS makes the role of HIV-1 unclear.

72 KS, nAb titers were similar between epidemic KS and endemic KS patients (P = 0.3).

73 polymerase chain reaction-confirmed epidemic KS and endemic KS patients and non-cancer controls from

74 d IL-10), nAb titers were higher in epidemic KS and endemic KS patients than in controls (P < .05).

75 Despite HIV-1 coinfection in epidemic KS, nAb titers were similar between epidemic KS and ende

76 secondary lymphoid tissues in an established KS (Kmt2d(+/betaGeo)) mouse model and validated select f

77 than those from GGAs or even from the exact KS potential.

78 L occurred at higher CD4 counts (P < .05 for KS and NHL) and with undetectable HIV RNA (P < .05 for K

79 ) and with undetectable HIV RNA (P < .05 for KS and NHL).

80 ys provides novel therapeutic approaches for KS tumors.

81 ion, providing novel therapeutic avenues for KS tumors.IMPORTANCE KSHV is the etiologic agent of Kapo

82 nd management in HIV clinics, especially for KS and cervical cancer, remain important priorities in t

83 ng cART, both incidence and risk factors for KS change with time since starting cART.

84 , SEPT6, NKRF, CX0rf57, NAA10, and FLNA) for KS are identified on Xq, as well as candidate central ge

85 Since current treatment methods for KS and PEL are fraught with unwanted side effects and lo

86 al of lipoxin using in vitro cell models for KS and PEL.

87 Newer treatments for KS based on the mechanisms of its pathogenesis are being

88 we examined whole-exome sequencing data from KS subjects.

89 Here we show that keratinocytes derived from KS patients are unable to undergo electrotaxis, and this

90 the 6 recipients who developed KS died from KS or associated complications.

91 mine whether consuming Lactobacillus gasseri KS-13, Bifidobacterium bifidum G9-1, and B. longum MM-2

92 a simple proof of a theorem: In generalized KS theory (GKS), the band gap of an extended system equa

93 ) theory is shown to be valid in generalized KS theory.

94 V LSSE and the sudden increases in H K and H KS at 175 K are associated with the spin reorientation d

95 e perpendicular magnetic anisotropy field (H KS) in the same Pt/YIG system.

96 e V LSSE peak at 75 K is attributed to the H KS and M S (saturation magnetization) whose peaks also o

97 es mL (median 72, range <50-74 375); all had KS and 2 also had PEL.

98 erved at low rates and were eclipsed by high KS and cervical cancer burden.

99 ngton, Maine, and California had the highest KS rates among PLWH.

100 ficient obese hyperglycemic/hyperinsulinemic KS db/db mouse model was used to assess consequential ef

101 KS) and in transplant recipients (iatrogenic KS).

102 onnector in HIV-KSHV interactions.IMPORTANCE KS is a prevalent tumor associated with infections with

103 In KS, differentially expressed escape genes are up-regulat

104 Pomalidomide is well tolerated and active in KS regardless of HIV status.

105 cteristic of NE tumors, both in vitro and in KS patient tissues and the heterogeneity of neuroendocri

106 Despite important ART-related declines in KS incidence, men and women in South Africa and men who

107 dlin-1 also failed to rescue electrotaxis in KS cells, indicating that both integrin and lipid bindin

108 ceptor/formyl peptidyl receptor (ALX/FPR) in KS patient tissue sections and in vitro KS and PEL cell

109 re no statistically significant increases in KS rates in any age, sex, or racial/ethnic group or in a

110 re no statistically significant increases in KS rates in any demographic or geographic group, nondecr

111 s and mechanisms of action of KSHV miRNAs in KS development.

112 iency have not previously been recognized in KS, and these results provide new mechanistic insights i

113 antiretrovirals, which frequently results in KS regression.

114 We estimated recent US trends in KS incidence among people living with human immunodefici

115 Incident KS patients aged 20-59 years were obtained from 36 cance

116 en who have sex with men remain at increased KS risk, likely due to high human herpesvirus 8 coinfect

117 erpesvirus-8), and viral proteins can induce KS-associated cellular changes that enable the virus to

118 tentially serve as markers for KSHV-infected KS lesion endothelial cells as well as novel therapeutic

119 NE genes HRH1 and NSE/ENO2 in KSHV-infected KS tissue samples and KS visceral tissue microarrays.

120 Interestingly, KS biosynthesis specific glycosyltransferases expression

121 The aetiologic agent of KS is KS herpesvirus (KSHV; also known as human herpesvirus-8)

122 biquitination of the kidney-specific isoform KS-WNK1 by the KLHL3-CUL3 complex rather than the long u

123 We successfully express 5 ketosynthase (KS) and chain length factor (CLF) pairs-e.g., from Photo

124 from a newly developed coupled ketosynthase (KS)-ketoreductase (KR) assay that established that the d

125 overexpressing kallistatin with OVE26 mice (KS-tg/OVE).

126 derlying pathogenic mechanism for this novel KS-associated variant.

127 The aetiologic agent of KS is KS herpesvirus (KSHV; also known as human herpesvi

128 Immunohistochemical analysis of KS expression was performed on primary pancreatic tumors

129 Herein, we report the first case of KS in a human immunodeficiency virus (HIV)-negative 47-y

130 We also briefly reviewed all the cases of KS in HIV-negative patients with inflammatory bowel dise

131 Currently, most cases of KS occur in sub-Saharan Africa, where KSHV infection is

132 Most cases of KS show a marked reduction or complete absence of the ki

133 of polymicrogyria are not characteristic of KS, and we found only a few previous reports of this ass

134 Kaposi sarcoma (KS) is a complication of KS-associated herpesvirus (KSHV) infection.

135 The main proliferating component of KS tumors is a cell of endothelial origin termed the spi

136 betic patients contributes to development of KS by promoting KSHV lytic replication and infection.

137 phases are important for the development of KS.

138 have an important role in the development of KS.

139 showed a mutation in COL18A1, diagnostic of KS.

140 MD-based binding energies of KS oligosaccharide-loaded galectins support experimental

141 harbored within a unique N-terminal exon of KS-WNK1.

142 tic tumors show a higher-level expression of KS compared to primary tumors.

143 fore, we aimed to identify the expression of KS epitope in human pancreatic cancer primary and metast

144 We observed an increased expression of KS epitope on primary tumor tissues compared to uninvolv

145 Recently, expression of KS in cancer has been shown to be highly associated with

146 results indicate that aberrant expression of KS is predictive of pancreatic cancer progression and me

147 ical specimen showed the typical findings of KS together with the HHV-8 positivity.

148 Reduced incidence of KS in HIV/AIDS patients receiving antiherpetic drugs to

149 The high incidence of KS in human immunodeficiency virus (HIV)-infected AIDS p

150 The incidence of KS in human immunodeficiency virus type 1-infected (HIV-

151 in system (RAS) upregulated in the kidney of KS-tg/OVE mice compared to WT/OVE mice, suggesting a dis

152 and erythropoietin levels in the kidneys of KS-tg/OVE mice.

153 s the fundamental gap, a major limitation of KS density-functional theory.

154 MLM is a modification of KS algorithm by adding a random-mutation factor.

155 ic potentialities and, in turn, the onset of KS.

156 echanistic insights into the pathogenesis of KS-associated immune deficiency.

157 cycle) is necessary for the pathogenesis of KS.

158 The clinical phenotype of KS includes moderate to severe intellectual disability w

159 An increasing proportion of KS and NHL occurred at higher CD4 counts (P < .05 for KS

160 be the relevance of molecular recognition of KS by galectins in terms of physiological processes in s

161 ata on Gal-3 and -7, and extend the scope of KS binding to Gal-1 and -9N.

162 e results demonstrate that the similarity of KS lesion cells to neuroendocrine tumors is probably a r

163 the mechanistic basis for the similarity of KS lesion endothelial cells to neuroendocrine tumors rem

164 new insight into the potential treatment of KS and PEL using nature's own anti-inflammatory molecule

165 One of the variants of KS is defined iatrogenic and is overall reported in tran

166 KIR influences the risk of KSHV infection or KS.

167 ed technique (Analyze Direct, Overland Park, KS).

168 ed controlled viremia with either persistent KS despite 3 months of antiretroviral therapy (ART) or p

169 tter awareness of the risk of posttransplant KS for recipients of organs from donors with HHV-8 infec

170 ed cells might lead to approaches to prevent KS development.

171 allenge to clearing infection and preventing KS development.

172 ermine whether ADCC has a role in preventing KS.

173 advanced (T1) disease, and 19 (86%) previous KS therapy excluding ART.

174 antiretroviral therapy (ART) or progressive KS despite 2 months of ART.

175 RT initiation in these children might reduce KS risk.

176 ell counts are essential to further reducing KS incidence worldwide, but additional measures might be

177 Treatment for early AIDS-related KS in previously untreated patients should start with th

178 tence reduced the prevalence of AIDS-related KS, although KS does occur in individuals with well-cont

179 opsy specimens compared with non-HIV-related KS and NST.

180 lated KS cases compared with non-HIV-related KS and NST.

181 32gamma isoforms was observed in HIV-related KS biopsy specimens compared with non-HIV-related KS and

182 oform, followed by IL-32beta, in HIV-related KS cases compared with non-HIV-related KS and NST.

183 o dietary potassium loading and restriction, KS-WNK1 knockout mice were deficient in these structures

184 RS, KS and MLM performance are compared in simulated and six

185 8) is the causative agent of Kaposi sarcoma (KS) and multicentric Castleman disease (MCD), a life-thr

186 Kaposi sarcoma (KS) can develop following organ transplantation through

187 Kaposi sarcoma (KS) gained public attention as an AIDS-defining malignan

188 Kaposi sarcoma (KS) had the highest IR (634.7 per 100 000 person-years)

189 The burden of Kaposi sarcoma (KS) in human immunodeficiency virus (HIV)-infected child

190 Kaposi sarcoma (KS) is a complication of KS-associated herpesvirus (KSHV

191 studies have suggested that Kaposi sarcoma (KS) rates might be increasing in some racial/ethnic grou

192 Kaposi sarcoma (KS) remains a frequent cancer in human immunodeficiency

193 We compared Kaposi sarcoma (KS) risk in adults who started antiretroviral therapy (A

194 V-related, 7 non-HIV-related Kaposi sarcoma (KS), and 7 normal skin tissues (NSTs) of Dutch origin we

195 V) is the causative agent of Kaposi sarcoma (KS), one of the leading cancers in human immunodeficienc

196 virus (KSHV) is the cause of Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and a form of Cast

197 ) is the causative agent for Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and multicentric C

198 pivotal role in controlling Kaposi sarcoma (KS)-associated herpesvirus (KSHV) and preventing disease

199 Kaposi sarcoma (KS)-associated herpesvirus (KSHV) is etiologically linke

200 Kaposi sarcoma (KS)-associated herpesvirus (KSHV) subtype depends mostly

201 rstanding of the burden of Kaposi's sarcoma (KS) and non-Hodgkin lymphoma (NHL) relative to antiretro

202 is the causative agent of Kaposi's sarcoma (KS) and other AIDS-related malignancies.

203 Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL) are two well-kno

204 is the etiologic agent of Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL).

205 ed malignancies, including Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL).

206 ed malignancies, including Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL).

207 Kaposi's sarcoma (KS) as the most common AIDS-associated malignancy is eti

208 Kaposi's sarcoma (KS) caused by oncogenic Kaposi's sarcoma-associated herp

209 ssociated with endothelial Kaposi's sarcoma (KS) in immunocompromised individuals.

210 Purpose Kaposi's sarcoma (KS) is a multicentric tumor caused by Kaposi's sarcoma-a

211 Kaposi's sarcoma (KS) is a rare vascular tumor associated with human herpe

212 High prevalence of Kaposi's sarcoma (KS) is seen in diabetic patients.

213 is the etiologic agent of Kaposi's sarcoma (KS), a vascular tumor frequently found in immunodeficien

214 is the etiologic agent of Kaposi's sarcoma (KS), an AIDS-defining cancer in HIV-1-infected individua

215 is the causative agent of Kaposi's sarcoma (KS), an AIDS-defining cancer with abnormal angiogenesis.

216 V) is the causal agent for Kaposi's sarcoma (KS), the most common malignancy in HIV/AIDS patients.

217 V) is the causal agent for Kaposi's sarcoma (KS), the most common malignancy in people living with hu

218 V), the causative agent of Kaposi's sarcoma (KS), to establish and maintain latency has been a major

219 Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is tightly linked with

220 rion production.IMPORTANCE Kaposi's sarcoma (KS)-associated herpesvirus is the causative agent of mul

221 several cancers, including Kaposi's sarcoma (KS).

222 genic virus that can cause Kaposi's sarcoma (KS).

223 is the etiologic agent of Kaposi's sarcoma (KS).

224 sed individuals, including Kaposi's sarcoma (KS).

225 ffusion lymphoma (PEL) and Kaposi's sarcoma (KS).

226 man herpesvirus 8 (HHV-8) (Kaposi's sarcoma [KS]-associated herpesvirus) and have an important role i

227 cture of the exact multiplicative Kohn-Sham (KS) potential substantially underestimates the fundament

228 pression for the work function in Kohn-Sham (KS) theory is shown to be valid in generalized KS theory

229 gistic regression and by Kolmogorov-Smirnov (KS) statistics.

230 In advanced-stage KS, chemotherapy with pegylated liposomal doxorubicin or

231 or geographic group, nondecreasing/stagnant KS trends in some states and among younger and black PLW

232 Age-standardized KS rates and annual percent changes (APCs) in rates were

233 random selection (RS) and the Kennard-Stone (KS) algorithms; here, the former works based on a random

234 s within the Upper Neosho River subdrainage, KS, from June-August 2013 yielded three generalizable ec

235 Keratan sulfate (KS) is a sulfated linear polymer of N-acetyllactosamine.

236 ize interactions of corneal keratan sulfate (KS), its desulfated form, as well as di-, tetra- (N-acet

237 rmatan sulfate (CS/DS), and keratan sulfate (KS)-mainly novel glycosylation strategies, elongation se

238 dulatory agent, in patients with symptomatic KS.

239 Kabuki syndrome (KS) is a complex multisystem developmental disorder asso

240 Kabuki syndrome (KS) is a congenital craniofacial disorder resulting from

241 Kabuki syndrome (KS) is commonly caused by mutations in the histone-modif

242 Because Kallmann syndrome (KS) is characterized by abnormal GnRH-1ns migration, we

243 Kindler syndrome (KS) is an autosomal recessive blistering skin disease re

244 Kleefstra syndrome (KS) (Mendelian Inheritance in Man (MIM) no.

245 rner syndrome (TS) and Klinefelter syndrome (KS) copy number aberrations of the X chromosome lead to

246 Knobloch Syndrome (KS) is a rare congenital syndrome characterized by occip

247 associated with anosmia (Kallmann syndrome, KS).

248 ite cysteine of a cognate ketoacyl synthase (KS).

249 toacyl-acyl carrier protein (ACP) synthases (KS), catalyze this process via a decarboxylative Claisen

250 The KS contact region involves the lectin canonical binding

251 The KS incidence rates were 0/100 000 PYs in children of non

252 The KS test is sensitive to variation in network scale, and

253 The KS was successfully treated by switching immunosuppressi

254 0% lower (adjusted OR, 0.6; P = .01) but the KS risk 80% higher with HLA-C group 1 homozygosity (adju

255 the combined cohorts, 0.6; P = .01), but the KS risk was 2-fold higher (adjusted OR, 2.1; P = .002).

256 distributions differed significantly by the KS test.

257 hose whose counts were <50 cells/microL, the KS risk was halved in South Africa (aHR, 0.53; 95% CI, .

258 o detailed molecular characterization of the KS-associated immune phenotype has been reported.

259 tic variants highlight the importance of the KS-WNK1 isoform abundance on potassium homeostasis.

260 yl-ACP binding and substrate delivery to the KS active site.

261 Over time, KS and NHL occurred at higher CD4 counts and lower HIV R

262 on in the host presents a major challenge to KS treatment or prevention.

263 itivity to electric fields and contribute to KS disease pathology.

264 rate that human GLI3 mutations contribute to KS etiology.SIGNIFICANCE STATEMENT The transcription fac

265 logical condition of diabetes contributes to KS development.

266 gene expression, ultimately contributing to KS development.

267 hat GLI3 is a candidate gene contributing to KS etiology.

268 d disrupted histone mark binding can lead to KS.

269 nhance KSHV dissemination and progression to KS if infection occurs.

270 o missense mutations in EHMT1 giving rise to KS have been described.

271 recipients were particularly susceptible to KS.

272 e and with that the risk for post-transplant KS.

273 on is one of the strategies adopted to treat KS and PEL, a primary motivation for exploring and evalu

274 dels offers a novel possibility for treating KS and PEL with lipoxins.

275 d to all KS forms, but mechanisms underlying KS development are unclear.

276 may help decipher the mechanisms underlying KS pathogenesis induced by HIV and KSHV coinfection.

277 ts with severe KSHV disease (2 with visceral KS, 1 with multicentric Castleman disease, and 1 with pr

278 ) in KS patient tissue sections and in vitro KS and PEL cell models offers a novel possibility for tr

279 tors involved in this process using in vitro KS and PEL cells as models.

280 We report a comparative analysis of TS vs. KS regarding differences at the genomic network level me

281 ver, ADCC responses were not associated with KS development or progression.

282 the virus-virus interaction associated with KS formation has focused on secretory factors.

283 n of the KSHV lytic cycle is associated with KS pathogenesis.

284 th complex medical histories consistent with KS in whom next generation sequencing identified the sam

285 Although several families with KS have been described previously, our case is noteworth

286 n is frequently observed in individuals with KS, but the role of KMT2D in immune system function has

287 more frequently detected in individuals with KS.

288 ed herpesvirus (KSHV) is tightly linked with KS, primary effusion lymphoma, and multicentric Castlema

289 munodeficiency virus (HIV)-infected men with KS, multicentric Castleman disease, or primary effusion

290 nd we find evidence of only one patient with KS who had an RD identified at an earlier age.

291 validated select findings in a patient with KS.

292 nction in a cohort (n = 13) of patients with KS (age, 4 months to 27 years).

293 V-8 MCD and compared them with patients with KS (n = 24) and healthy donors (n = 29).

294 We identified 466 patients with KS and 258 with NHL.

295 All patients with KS should undergo serial clinical immune evaluations.

296 umoral immune defects found in patients with KS with lysine methyltransferase 2D (KMT2D) mutations.

297 In patients with KS, autosomal dominant KMT2D mutations are associated wi

298 Chemical probes capable of reacting with KS (ketosynthase)-bound biosynthetic intermediates were

299 RESENTATIONS: We report on two siblings with KS.

300 hort of HIV-infected Zambian mothers without KS and identify potential factors that may influence tra

301 Here, we show that kidney-specific WNK1 (KS-WNK1), a truncated kinase-defective WNK1 isoform that

302 In recent years, KS was more frequently diagnosed after ART initiation (5