ライフサイエンスコーパス: podocyte

1 in dye in different cell types including the podocyte.

2 dially arranged toward periphery of expanded podocyte.

3 within the target cell for FSGS, the kidney podocyte.

4 ctions were investigated in primary cultured podocytes.

5 its in vitro-functional significance injured podocytes.

6 at microtubules at primary processes in rat podocytes.

7 2-CAAX isoform is the predominant isoform in podocytes.

8 imulates phosphorylation of ACTN4 at S159 in podocytes.

9 ide exchange factor plays a critical role in podocytes.

10 of the cognate gene, SPOCK2, exclusively in podocytes.

11 ge factor that interacts with Cdc42 in human podocytes.

12 ed by antibody accessibility, in serum or on podocytes.

13 ing dynein-mediated vesicular trafficking in podocytes.

14 ced calcium transients in significantly more podocytes.

15 organization and stabilization in glomerular podocytes.

16 ore, TrkC modulates Igf-related signaling in podocytes.

17 recombinant uPAR on primary culture of human podocytes.

18 and adhesion-characteristics of TRPC6 (-/-) podocytes.

19 are believed to involve injury to glomerular podocytes.

20 the Igf1R on activating tyrosine residues in podocytes.

21 rs that activate Cdc42 in immortalized human podocytes.

22 ormal gene expression was pinpointed in late podocytes.

23 is phosphorylated at serine (S) 159 in human podocytes.

24 nic human SRNS due to actin dysregulation in podocytes.

25 a formation in shRNA-induced DAAM2-knockdown podocytes.

26 cal for the normal development and health of podocytes.

27 f the structural and functional integrity of podocytes.

28 plicated in monogenic glomerular diseases in podocytes.

29 In the glomerular podocytes, accumulation of GL3 progresses with age.

30 on in the expression of nephrin, significant podocyte actin cytoskeleton, and motility changes.

31 tes and the protein transmits signals to the podocyte actin cytoskeleton.

32 odocyte foot process effacement of remaining podocytes, activation of proximal tubule-like parietal e

33 rular ROBO2 expression that might compromise podocyte adhesion and, thus, loss of Robo2 in podocytes

34 protect from glomerular injury by enhancing podocyte adhesion that helps maintain foot process struc

35 myosin IIA activity, and destabilizes kidney podocyte adhesion.

36 n of miR-466o-3p was upregulated in cultured podocytes after beta-catenin activation and in glomerula

37 ing acute activation of the Hippo pathway in podocytes after nephrotoxic immune injury.

38 ney disease through its selective binding to podocyte alphavbeta3 integrin.

39 Both endogenous podocyte and transfected APOL1 isoforms vA and vB1 (and

40 rganoids cultured under flow had more mature podocyte and tubular compartments with enhanced cellular

41 Urinary pellet podocyte and tubular mRNA markers were increased in all

42 We utilized a primary culture of human podocytes and 2 mouse models, the wild type (WT) and the

43 of the DID-containing N-terminal fragment in podocytes and assessed whether the FSGS-associated R218Q

44 in (Synpo) is an actin-associated protein in podocytes and dendritic spines.

45 APOL1 is found in human kidney podocytes and endothelia.

46 We examined INF2 isoforms present in podocytes and evaluated INF2 cleavage as an explanation

47 preventing the loss of proteins, using human podocytes and glomerular endothelial cells seeded into m

48 nsulin-resistant vs. insulin-sensitive mouse podocytes and in human glomeruli of patients with early

49 how that DAAM2 localizes to the cytoplasm in podocytes and in kidney sections.

50 to several normal tissues, including kidney podocytes and lymphatic endothelial cells but not vascul

51 human glomeruli that were composed mainly of podocytes and mesangial cells.

52 However, the capacity for autophagy in both podocytes and renal tubular cells is markedly impaired i

53 diminution in autophagic flux in glomerular podocytes and renal tubules and markedly increasing thei

54 mprises a glomerular vasculature embraced by podocytes and supported by mesangial myofibroblasts, whi

55 tabilization of the slit diaphragm of mature podocytes and that autoantibodies to THSD7A, on the basi

56 ine kinase receptor 3 (TrkC) is expressed in podocytes and the protein transmits signals to the podoc

57 Hdg, a byproduct of oxidative DNA damage) in podocytes and tubular epithelial cells.

58 ylation-based trafficking assays in cultured podocytes, and a new puromycin aminoglycoside nephropath

59 yrosine phosphorylation response in CD2AP in podocytes, and that these phosphorylation events have an

60 It is unclear where endogenous podocyte APOL1 resides, because previous immunolocalizat

61 In kidneys of G6PD-deficient mice, podocyte apoptosis was significantly increased.

62 Loss of beta-PIX promoted podocyte apoptosis, which was mediated by the reduced ac

63 n of G6PD with small interfering RNA induced podocyte apoptosis.

64 beta-PIX is required for the maintenance of podocyte architecture and glomerular function via Cdc42

65 Human podocytes are highly sialylated; however, sialylation's

66 Podocytes are highly specialized cells that play an esse

67 regulatory mechanisms for Cdc42 activity in podocytes are largely unknown.

68 Compared with wild-type cells, TRPC6(-/-) podocytes are less motile and more adhesive, with an alt

69 Podocytes are pivotal in establishing the selective perm

70 Of concern, podocytes are relatively resistant to enzyme replacement

71 idney cell lines and the sarcoma cells; only podocytes are significantly less affected by LCA (at dos

72 sion of THSD7A and its biologic function for podocytes are unknown, information that is needed to und

73 n beta1 at focal adhesions, which may affect podocyte attachment to the extracellular matrix.

74 Our discovery that podocytes become sensitized to AngII-induced calcium sig

75 in podocytes deepening our understanding of podocyte biology and disease.

76 aster regulators that play opposing roles in podocyte biology and mutually antagonize each other.

77 we focus on the role of nuclear receptors in podocyte biology and non-diabetic glomerular disease.

78 gG did not interfere with its entry into the podocytes but eliminated its ability to upregulate CAMK4

79 tial channel 6, which has been implicated in podocyte calcium handling.

80 To study the effects of AngII on podocyte calcium levels in vivo, we used intravital micr

81 In contrast to previous findings, podocytes can function normally in vivo in the absence o

82 e transcription of HPS1, 3, 4 and 5 in human podocyte cell culture, suggesting that impaired function

83 ro experiments using Tcf21-expressing murine podocyte cell line, we could observe some Tcf21-dependen

84 Our snRNA-seq protocol yielded 20-fold more podocytes compared with published scRNA-seq datasets (2.

85 y, overexpression of ROBO2 in cultured mouse podocytes compromises cell adhesion.

86 APOL1 knockout podocytes confirmed antibody specificity.

87 odocyte adhesion and, thus, loss of Robo2 in podocytes could protect from glomerular injury by enhanc

88 reporter mouse model to establish a primary podocyte culture system.

89 vo transcriptional response from the primary podocyte culture with glomerular transcripts across a wi

90 Podocyte GL3 volume fraction (proportion of podocyte cytoplasm occupied by GL3) increased with age u

91 agonism using thiazolidinediones has potent podocyte cytoprotective and nephroprotective effects.

92 n of calpain activity; this leads to altered podocyte cytoskeleton, motility, and adhesion-characteri

93 Proposed mechanisms of kidney podocyte cytotoxicity resulting from APOL1 variant overe

94 ession of glomerulosclerosis involve loss of podocyte DAF, triggering local, complement-dependent, IL

95 podocin-encoding gene Nphs2, the consequent podocyte damage and proteinuria rendered the cells respo

96 wever, the exact mechanism of APOL1-mediated podocyte damage is not clear, including APOL1's subcellu

97 oup of patients with proteinuria, indicating podocyte damage.

98 uPAR did not result in podocytes damage.

99 al Fc Receptor (FcRn) or CAMK4 prevented the podocyte-damaging effects of IgG from patients with TG.

100 e novel [Ca(2+) ] regulated gene networks in podocytes deepening our understanding of podocyte biolog

101 excretion correlated highly with decreasing podocyte density (R(2) = 0.86), as a consequence of both

102 Glomerular podocyte density gradually decreased in podocyte-specifi

103 ive effects on DeltaGFR, glomerulosclerosis, podocyte density in juxtamedullary nephrons, and filtrat

104 BIO alone improved albuminuria, podocyte density in superficial and juxtamedullary nephr

105 verlapping AUC contributions, as expected if podocyte depletion causes albuminuria.

106 indings indicate that glomerular response to podocyte depletion in larval zebrafish resembles human F

107 ether, our findings identify testican-2 as a podocyte-derived biomarker of kidney health and prognosi

108 Individual podocyte descriptors such as effacement and microvillous

109 (Urinary pellet podocin:nephrin mRNA ratio), podocyte detachment (Urinary pellet podocin mRNA:creatin

110 In the podocyte differentiation process described here, hPSCs a

111 in human glomeruli, and affected individual podocytes displayed architectural changes associated wit

112 In healthy animals, podocytes displayed limited responsiveness to AngII stim

113 APOL1 knockout podocytes do not stain for APOL1, attesting to the APOL1

114 erular FSGS tissue and purified native mouse podocytes during early disease stages.

115 Hyperglycemia-induced podocyte dysfunction is a major contributor of renal fun

116 ng suPAR as a pathophysiological mediator in podocyte dysfunction.

117 d c-Jun N-terminal kinase (JNK) activity and podocyte dysfunction.

118 miR-466o-3p alleviated beta-catenin-induced podocyte dysfunction.

119 In our monogenic podocyte ER stress-induced NS/FSGS mouse model, the podo

120 Interestingly, organoid-generated podocytes exhibited highly similar, progressive transcri

121 Phosphomimetic Actn4 mouse podocytes exhibited more spatially correlated F-actin al

122 en and young adults, genetic variants in >50 podocyte-expressed genes, syndromal non-podocyte-specifi

123 human showed a positive correlation with its podocyte expression level.

124 Here, we show that podocyte expression of decay-accelerating factor (DAF/CD

125 aggregating in, and inhibiting motility of, podocytes, fibroblasts and melanoma cells.

126 inuria, and glomerulosclerosis and increased podocyte filtration slit density, as assessed by STED su

127 superficial and juxtamedullary nephrons, and podocyte filtration slit density.

128 function but mitigated hypertension-induced podocyte foot process effacement and albuminuria.

129 Additionally, we observed severe podocyte foot process effacement of remaining podocytes,

130 ogical changes were associated with profound podocyte foot process effacement, cell death, and sustai

131 hat Shroom3 knockdown led to albuminuria and podocyte foot process effacement.

132 , electron microcopy analyses showed a focal podocyte foot process effacement.

133 the N-terminal region normally localizes to podocyte foot processes, it does not do so in the presen

134 into podocytes has the potential to produce podocytes for disease modeling, drug screening, and cell

135 confocal and immunoelectron microscopy, and podocyte fractionation localized endogenous and transfec

136 Proteome analysis of purified podocyte fractions from FSGS mouse models showed an earl

137 disease states in FSGS mouse models, we used podocyte fractions isolated from individual mice after c

138 e analysis to very small samples of purified podocyte fractions.

139 In cultured primary podocytes from mutant mice, the absence of Synpo caused

140 runcated version (Synpo-T) is upregulated in podocytes from Synpo mutant mice.

141 ets for therapeutic intervention to preserve podocyte function following glomerular injury.

142 gen Synthase Kinase 3 (GSK3) for maintaining podocyte function in mice and the equivalent nephrocyte

143 lasts, which ensure plasma filtration at the podocyte-generated slit diaphragm.

144 Podocyte GL3 volume fraction (proportion of podocyte cyt

145 g podocyte structural parameters (increasing podocyte GL3 volume fraction and foot process width) was

146 to about age 27, suggesting that increasing podocyte GL3 volume fraction beyond a threshold may comp

147 been suggested, a direct effect of AngII on podocytes has not been demonstrated in vivo.

148 of human pluripotent stem cells (hPSCs) into podocytes has the potential to produce podocytes for dis

149 y of the target cell in INS - the glomerular podocyte - has transformed our understanding of the mech

150 podocalyxin is ablated (immature vs. mature podocytes) has a profound effect on the urinary phenotyp

151 that provides structural support for kidney podocytes-have been linked to proteinuric glomeruloscler

152 nical implications of mitotic catastrophe in podocyte health during diabetic kidney disease.

153 entity is injury and ultimately depletion of podocytes, highly arborized interdigitating cells on the

154 y sialylated; however, sialylation's role in podocyte homeostasis remains unclear.

155 [Ca(2+) ] and the actin cytoskeleton play in podocyte homeostasis.

156 Thus, the limited supply of primary podocytes impedes CKD research.

157 er beta-catenin activation and in glomerular podocytes in adriamycin (ADR) nephropathy, remnant kidne

158 Increased expression of Filamin-B in podocytes in biopsy samples from patients with FSGS, in

159 e report that SMPDL3b excess, as observed in podocytes in diabetic kidney disease (DKD), impairs insu

160 To examine podocytes in early disease states in FSGS mouse models,

161 ell-lines, sparing the highly differentiated podocytes in lower concentrations.

162 prevent excessive APOL1 expression in human podocytes in response to nsDNA.

163 he present article, using immortalized human podocytes in vitro and a mouse model in vivo, we show th

164 phosphate (C1P) content as observed in human podocytes in vitro and in kidney cortexes of diabetic db

165 romoted CFH expression in immortalized mouse podocytes in vitro.

166 In nephrotic rat models, TCF21 expression in podocytes increased along with the severity of nephrotic

167 at in response to sublytic levels of injury, podocyte induced CFH expression locally and clearance of

168 ROBO2 is expressed in podocytes, inhibits nephrin-induced actin polymerization

169 stic studies show that C3a/C3aR ligations on podocytes initiate an autocrine IL-1beta/IL-1R1 signalin

170 In immunotoxin (LMB2) induced fatal podocyte injury (NEP25/LMB2) at day 12, glomerular CFH a

171 ors and obesity are also important causes of podocyte injury and frequently combine to cause various

172 , this study points to an important role for podocyte injury and loss in the progression of Fabry nep

173 GL3 accumulation was associated with podocyte injury and loss, as evidenced by increased foot

174 Levels of albuminuria, podocyte injury and podocyte number were similar in the

175 ggest that ROBO2 is a therapeutic target for podocyte injury and podocytopathy.

176 nic mechanism by which beta-catenin promotes podocyte injury and proteinuria in glomerular diseases.

177 ACTN4 may mediate podocyte injury as a consequence of both genetic mutatio

178 This study reveals podocyte injury as main cause of proteinuria in hantavir

179 -466o-3p in mediating beta-catenin-triggered podocyte injury by targeting WT1.

180 levels of glomerular ceramide with decreased podocyte injury compared with Asah1(fl/fl)/Podo(Cre) mic

181 kidney diseases in which direct or indirect podocyte injury drives proteinuria or nephrotic syndrome

182 Podocyte injury has recently been described as unifying

183 neralocorticoid receptor modulators regulate podocyte injury in experimental models.

184 isingly reduced the level of albuminuria and podocyte injury in models of both diabetic and nondiabet

185 n is sufficient to attenuate proteinuria and podocyte injury in mouse models of diabetes.

186 results offer novel considerations to limit podocyte injury in patients with kidney transplants, whi

187 The mechanisms that lead to podocyte injury in TG remain unclear.

188 monstrates a role for plasmin (ogen)-induced podocyte injury in the PAN nephropathy model, with amilo

189 6o-3p downregulated WT1 protein and promoted podocyte injury in vitro.

190 Finding a window into early podocyte injury might help identify molecular pathways i

191 In addition, puromycin-induced sublytic podocyte injury promoted CFH expression in immortalized

192 po plays a protective role in the context of podocyte injury through its involvement in actin reorgan

193 lobulin G [IgG]), urinary nephrin excretion (podocyte injury) and serum levels of the soluble urokina

194 ng less albuminuria, glomerular hypertrophy, podocyte injury, and interstitial fibrosis compared with

195 hannel model for APOL1 risk variant-mediated podocyte injury, as well as providing domain accessibili

196 onflicting results on the effect of suPAR on podocyte injury, effacement of foot processes, and prote

197 suPAR by itself is not the cause for direct podocyte injury, in vitro or in vivo.

198 The mice manifested podocyte injury, including c-Src phosphorylation, protei

199 ocal, complement-dependent, IL-1beta-induced podocyte injury, potentially identifying new therapeutic

200 hypothesized that PUUV infection results in podocyte injury, similar to findings in INS.

201 ed its ability to upregulate CAMK4 and cause podocyte injury.

202 river of nephrotoxicity and specifically, of podocyte injury.

203 remodeling contributes to ER stress-induced podocyte injury.

204 ion of miR-466o-3p inhibited WT1, aggravated podocytes injury and deteriorated proteinuria.

205 tion, substantially restored WT1, alleviated podocytes injury and reduced renal fibrosis.

206 post-translational modifications of ACTN4 on podocyte integrity and kidney function is not known.

207 , phenotypically, THSD7A expression in human podocytes is associated not only with increases in cell

208 esults strongly suggest that lysosomal Ac in podocytes is essential for the maintenance of the struct

209 ther studies reveal that ROBO2 expression in podocytes is up-regulated after glomerular injury becaus

210 during kidney injury, particularly in mature podocytes, is not known.

211 Here, we studied the transcriptomes of podocytes, key cells in the prevention of albuminuria, u

212 c1d8b in Drosophila impaired function of the podocyte-like nephrocytes, and caused mistrafficking of

213 th peripheral blood sample and urine-derived podocyte-lineage cells unmasked the COL4A5 mutation only

214 lls unmasked the COL4A5 mutation only in the podocyte-lineage cells.

215 Given the known association between podocyte loss and irreversible FSGS and global glomerulo

216 for therapeutic intervention before critical podocyte loss occurs.

217 s level is difficult because injury leads to podocyte loss or an increase of extracellular matrix, al

218 , basement membrane thickening, albuminuria, podocyte loss, and aspects of FSGS during aging.

219 creatinine ratio in TG signifies accelerated podocyte loss.

220 -specific beta-PIX knockout mice, indicating podocyte loss.

221 In podocytes, loss of Dnmt1, Dnmt3a, Dnmt3b, or Tet2 did no

222 Podocyte markers and albuminuria had overlapping AUC con

223 ound in individuals with NS, rescued reduced podocyte migration rate (PMR) and restored reduced filop

224 iHB prevented renal dysfunction and reversed podocyte migration rate impairment.

225 ng expression of podocyte-specific genes and podocyte morphology.

226 y immunofluorescence of differentiated mouse podocytes (MPCs), dynamin 1 was often colocalized with m

227 The hypothesis that urinary pellet podocyte mRNA is a more sensitive progression risk marke

228 In vitro, podocyte NPY signaling occurred via the NPY2 receptor (N

229 omerular volume (R(2) = 0.70) and decreasing podocyte number (R(2) = 0.63).

230 docyte stress and injury) and with decreased podocyte number density per glomerular volume.

231 Levels of albuminuria, podocyte injury and podocyte number were similar in the sirolimus and vehicl

232 ified by the fact that CAMK4 is increased in podocytes of patients with TG but not in those without T

233 on electron microscopic analysis showed that podocytes of the knockout mice had distinctive foot proc

234 glomerular endothelial cells and not in the podocytes of WT mice and was not detected at the uPAR KO

235 Injury to kidney podocytes often results in chronic glomerular disease an

236 diated transport of nephrin in R218Q knockin podocytes opens an avenue for developing targeted therap

237 ), did not induce proteinuria, effacement of podocytes, or disruption of the cytoskeleton.

238 of uEV analysis such as autofluorescence of podocyte origin.

239 ns some Synpo functions, which may prevent a podocyte phenotype from emerging in unchallenged mutant

240 In cultured human podocytes, plasminogen treatment was associated with dec

241 o when overexpression was induced locally in podocytes (podVEGFC) in otherwise healthy mice.

242 that deletes Podxl in developmentally mature podocytes (Podxl(DeltaPod)) and a second that is heteroz

243 ously published studies in mice and isolated podocytes produced conflicting results on the effect of

244 ich exert their immunosuppressive and direct podocyte protective effects via the glucocorticoid recep

245 PAN nephropathy model, with amiloride having podocyte-protective properties.

246 o-PPXY motif polypeptide of the synaptic and podocyte protein synaptopodin (SYNPO).

247 system (RAS), is predominantly presented in podocytes, proximal tubules, distal convoluted tubules,

248 loss of a single Nphs2 allele also increased podocytes' responsiveness to AngII signaling.

249 This direct effect of AngII on injured podocytes results in increased calcium transients, which

250 Herein, we report that loss of ROBO2 in podocytes [Robo2 conditional knockout (cKO) mouse] is pr

251 Thus, podocyte RyR2 remodeling contributes to ER stress-induce

252 Dasatinib treated podocytes show significant changes in focal adhesions, a

253 Dynamins 1 and 2 double-knockout podocytes showed dispersed acetylated alpha-tubulin and

254 hnology was used to assess for detachment of podocytes simultaneously exposed to fluid flow and cycli

255 ury and as a viable targetable biomarker for podocyte-sparing treatments.

256 c POD-ATTAC mice, which display an inducible podocyte-specific apoptosis.

257 We generated podocyte-specific ARHGEF7 (commonly known as beta-PIX) k

258 Compared with controls, glomeruli from podocyte-specific beta-PIX knockout mice and cultured mo

259 Podocyte-specific beta-PIX knockout mice developed progr

260 ular podocyte density gradually decreased in podocyte-specific beta-PIX knockout mice, indicating pod

261 mouse strain (Asah1(fl/fl)/Podo(Cre)) with a podocyte-specific deletion of the alpha subunit (main ca

262 nephrotic syndrome in mice bearing the Asah1 podocyte-specific gene deletion.

263 >50 podocyte-expressed genes, syndromal non-podocyte-specific genes and phenocopies with other under

264 disease progression, including expression of podocyte-specific genes and podocyte morphology.

265 with FSGS revealed an underrepresentation of podocyte-specific genes and proteins in late-stage disea

266 In vivo studies were carried out in a podocyte-specific Gprc5b knockout mouse line.

267 teinuria and albuminuria were found in these podocyte-specific knockout mice compared with control ge

268 Understanding podocyte-specific responses to injury at a systems level

269 Podocyte stress (Urinary pellet podocin:nephrin mRNA rat

270 h (a generally accepted structural marker of podocyte stress and injury) and with decreased podocyte

271 We identified conserved mechanisms of the podocyte stress response through ultrasensitive proteome

272 identify molecular pathways involved in the podocyte stress response.

273 Worsening podocyte structural parameters (increasing podocyte GL3

274 topology in serum (HDL particles) and at the podocyte surface.

275 ADR induces enzymatic cleavage of DAF from podocyte surfaces, leading to complement activation.

276 -oxime (BIO), previously reported to promote podocyte survival and regeneration, is a candidate addit

277 servations highlight a detrimental effect of podocyte-targeted HO-1 overexpression on ageing-related

278 We treated these podocytes temporarily with a Calcium Ionophore and facul

279 , Gprc5b, as a novel gene highly enriched in podocytes that was significantly upregulated in common h

280 In podocytes, the N-fragment localizes to the plasma membra

281 cular and structural features with mammalian podocytes, they provide an efficient model for studying

282 Li et al that links ceramide accumulation in podocytes to cellular damage and nephrotic syndrome.

283 sis identified a transcriptional response in podocytes to elevated [Ca(2+) ] levels, affecting mRNA l

284 the extracellular domain, was endocytosed by podocytes to induce apoptosis and glomerular dysfunction

285 roteinuric patients and exposure of cultured podocytes to plasminogen results in injury via oxidative

286 ceptor signaling were enriched in lysates of podocytes treated with the TrkC ligand neurotrophin-3 (N

287 e ER stress-induced NS/FSGS mouse model, the podocyte type 2 ryanodine receptor (RyR2)/calcium releas

288 in both the formation and the maintenance of podocyte ultrastructure.

289 ated inflammation in renal tubular cells and podocytes under hyperglycemic conditions.

290 ngle glomeruli from proteinuric rats, and in podocytes undergoing mechanical stress suggests that thi

291 Underlying mechanisms include podocyte (visceral glomerular epithelial cell/GEC) injur

292 ology in serum (HDL particles) and in kidney podocytes was mapped with flow cytometry, immunoprecipit

293 e of [Ca(2+) ] and the actin cytoskeleton in podocytes, we used a double fluorescent reporter mouse m

294 In a transgenic zebrafish strain, podocytes were depleted, and the glomerular response was

295 ulointerstitial lesions were prominent while podocytes were edematous with areas of foot process effa

296 d RC 124 from adult kidney tissue as well as podocytes were used.

297 aused defective formation of lamellipodia in podocyte, which would lead to the disruption of slit dia

298 Using shRNA, we established cultured mouse podocytes with beta-PIX knockdown and their controls.

299 ic beta-PIX knockout mice and cultured mouse podocytes with beta-PIX knockdown exhibited significant

300 Stable re-transfection of knockout podocytes with inducible APOL1-G0, -G1, and -G2 showed n

301 APOL1 localizes to the surface of podocytes, with most of the pore-forming domain (PFD) an