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1 id oxidation (FAO) in the pericardial cells (nephrocytes).
2 s markedly impair filtration function in the nephrocyte.
3 cells, primary patient cells, and Drosophila nephrocytes.
4 tors were silenced using RNA interference in nephrocytes.
5 tissue and is taken up by renal cells called nephrocytes.
6 in early endosomal structures in Drosophila nephrocytes.
7 slit diaphragms in podocyte-like Drosophila nephrocytes.
8 ing to genetic interaction of sns and c3g in nephrocytes.
9 expressed at the lacuna channel membranes of nephrocytes.
10 e invaginated membranes (lacuna channels) of nephrocytes.
11 , the reabsorptive hindgut and the endocytic nephrocytes.
12 reduced filtration function in the affected nephrocytes.
13 podin, was also elevated in Bazooka depleted nephrocytes.
14 s, garland nephrocyte cells, and pericardial nephrocytes.
15 rug screening using podocyte-like Drosophila nephrocytes.
16 like junctions between abnormally aggregated nephrocytes.
17 ene in vitro and in podocyte-like Drosophila nephrocytes.
18 nephrotic syndrome have not been studied in nephrocytes.
19 enotype reminiscent of nephrotic syndrome in nephrocytes.
20 diomyopathy that developed in the absence of nephrocytes.
21 hrin and Neph1, respectively, in pericardial nephrocytes.
22 on of the fluorescent protein in pericardial nephrocytes.
23 rise to cardioblasts, blood progenitors and nephrocytes.
24 in podocytes or the nephrocyte diaphragm in nephrocytes.
25 Expressing the G0 or G1 APOL1 transgene in nephrocytes also impaired the acidification of organelle
26 O-1 (TJP1) and podocin, are expressed in the nephrocyte and form a complex of interacting proteins th
28 tch that differentiates between the blood or nephrocyte and vascular lineages involves the Notch path
30 Here, we present a functional analysis of nephrocytes and establish an in vivo system to screen fo
31 n was required for rapid nephrin turnover in nephrocytes and for endocytosis of nephrin induced by ex
34 important role in the calcium homeostasis of nephrocytes and is required for maintaining nephrocyte f
35 irculatory system: cardioblasts, pericardial nephrocytes and lymph gland hematopoietic progenitors, b
36 complex proteins specifically in Drosophila nephrocytes and studied the effects on protein reabsorpt
37 loss-of-function strategy was used to ablate nephrocytes and then heart function and the hemolymph pr
38 , we conducted genetic studies in Drosophila nephrocytes and validated findings from Drosophila in a
39 imilarities we describe between invertebrate nephrocytes and vertebrate podocytes provide evidence su
40 and Pannier in cardioblasts and pericardial nephrocytes, and by Serpent in hematopoietic progenitors
41 phila impaired function of the podocyte-like nephrocytes, and caused mistrafficking of Sns, the Droso
42 la Vps8 is highly expressed in hemocytes and nephrocytes, and localizes to early endosomes despite th
43 els lacking Rab7 exclusively in podocytes or nephrocytes, and performed histologic and ultrastructura
47 re evolutionarily related, and establish the nephrocyte as a simple model in which to study podocyte
48 podocytes and an ex vivo model of Drosophila nephrocytes, as well as chemically induced injury models
50 STAT signaling pathway in the adipose tissue-nephrocyte axis and its contribution to HFD-associated n
53 on of APOL1 risk variants in D. melanogaster nephrocytes caused cell-autonomous accumulation of the e
56 factor Klf15 (Klf15(NN)) are viable but lack nephrocytes-cells structurally and functionally homologo
58 late the structure and function of the SD in nephrocytes, connecting the SD protein complex to the ac
62 rivation or antibiotic treatment ameliorates nephrocyte deterioration and extends the lifespan of tum
63 ph by uptake of molecules through an SD-like nephrocyte diaphragm (ND) into labyrinthine channels tha
64 structure revealed that the formation of the nephrocyte diaphragm and lacunar structure, which is ess
65 ermore, gene silencing of c3g partly rescued nephrocyte diaphragm defects of an sns overexpression ph
75 eath and direct ER stress induction enhanced nephrocyte endocytic function similar to expression of A
81 fic gene silencing of sns or c3g compromised nephrocyte filtration and caused nephrocyte diaphragm de
86 xpression of the APOL1 G0 or G1 transgene in nephrocytes, fly cells homologous to mammalian podocytes
90 nephrocytes and is required for maintaining nephrocyte function and the slit diaphragm filtration st
91 ed a faster but reliable screening assay for nephrocyte function compared with the established approa
92 As transgenic flies with either allele aged, nephrocyte function declined, cell size increased, and n
95 ion of an APOL1 transgene initially enhances nephrocyte function, causing hypertrophy and subsequent
96 We developed a fast assay testing Drosophila nephrocyte function, suitable for whole-animal drug scre
101 cells and oenocytes (also called Drosophila nephrocytes) function in taking up waste material from t
104 lencing Cindr in nephrocytes led to dramatic nephrocyte functional impairment and shortened life span
105 und that 85% of these genes are required for nephrocyte functions, suggesting that a majority of huma
106 co-expressed within binucleate garland cell nephrocytes (GCNs) that contribute to detoxification of
107 Mature genetic or pharmacological podocyte/nephrocyte GSK3 inhibition is also detrimental; producin
112 nephrin colocalized at the slit diaphragm in nephrocytes in a mutually dependent manner, interacting
114 data suggest that the Drosophila pericardial nephrocyte is a useful in vivo model to help identify ge
117 shortened life span, as well as collapse of nephrocyte lacunar channels and effacement of nephrocyte
121 on microscopy showed that silencing Piezo in nephrocytes led to reduced slit diaphragm density and ab
125 te, but the lack of a functional readout for nephrocytes makes it challenging to study this model of
129 , we study nephrin dynamics in podocyte-like nephrocytes of Drosophila and show that selective endocy
131 hosts, as blocking the NF-kB/Imd pathway in nephrocytes or removing gut bacteria via germ-free deriv
135 hannel activity, does not result in a severe nephrocyte phenotype, suggesting the observed changes in
143 uggest that the slit diaphragm of Drosophila nephrocytes requires balanced endocytosis and recycling
144 ull allele of Drosophila TBC1D8B exhibited a nephrocyte-restricted phenotype of nephrin mislocalizati
145 Loss of function analysis in Piezo depleted nephrocytes reveal a severe morphological and functional
147 erular basement membrane model in Drosophila nephrocytes reveals that matrix receptor-mediated cues e
152 es reduced the density of slit diaphragms in nephrocytes, showing a direct effect of the matrix.
155 d fluorescent protein and combined it with a nephrocyte-specific driver for targeted gene knockdown,
157 ice and Drosophila with podocyte-specific or nephrocyte-specific loss of Rab7, and a human podocyte c
159 ulation was found at garland and pericardial nephrocytes supporting its role in organismal defence an
160 ch are pairs of highly endocytic pericardial nephrocytes that modulate cardiac function by uncharacte
161 o elevate endocytic function of garland cell nephrocytes that simultaneously showed early signs of ce
163 s the slit diaphragm filtration structure in nephrocytes, the fly functional equivalent of mammalian
166 can was removed from systemic circulation by nephrocytes through endocytosis and subsequent lysosomal
167 tion in primary patient cells and Drosophila nephrocytes to systematically characterize a large panel
168 bsorption is required for the maintenance of nephrocyte ultrastructure and fly survival under conditi
169 stic syndrome model, wherein the pericardial nephrocytes undergo severe damage due to an elevated imm
170 rgeted expression of human AMN in Drosophila nephrocytes was sufficient to rescue defective protein u
171 Using RNAi and conditional CRISPR/Cas9 in nephrocytes, we found this pattern depends on the expres
172 pression of dCubilin and dAMN is specific to nephrocytes, where they function as co-receptors for pro
173 ctional genetic screen of Drosophila cardiac nephrocytes, which are equivalents of mammalian podocyte
175 e that HFD activates the JAK-STAT pathway in nephrocytes, which has previously been linked to diabeti
176 g apicobasal polarity proteins in Drosophila nephrocytes, which have SDs similar to those of mammalia
177 system, consisting of Malpighian tubules and nephrocytes, which shares similarities with the mammalia