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1 s markedly impair filtration function in the nephrocyte.
2 enotype reminiscent of nephrotic syndrome in nephrocytes.
3 diomyopathy that developed in the absence of nephrocytes.
4 nephrotic syndrome have not been studied in nephrocytes.
5 hrin and Neph1, respectively, in pericardial nephrocytes.
6 on of the fluorescent protein in pericardial nephrocytes.
7 rise to cardioblasts, blood progenitors and nephrocytes.
8 in podocytes or the nephrocyte diaphragm in nephrocytes.
9 Expressing the G0 or G1 APOL1 transgene in nephrocytes also impaired the acidification of organelle
10 O-1 (TJP1) and podocin, are expressed in the nephrocyte and form a complex of interacting proteins th
12 tch that differentiates between the blood or nephrocyte and vascular lineages involves the Notch path
13 Here, we present a functional analysis of nephrocytes and establish an in vivo system to screen fo
16 irculatory system: cardioblasts, pericardial nephrocytes and lymph gland hematopoietic progenitors, b
17 loss-of-function strategy was used to ablate nephrocytes and then heart function and the hemolymph pr
18 imilarities we describe between invertebrate nephrocytes and vertebrate podocytes provide evidence su
19 and Pannier in cardioblasts and pericardial nephrocytes, and by Serpent in hematopoietic progenitors
20 la Vps8 is highly expressed in hemocytes and nephrocytes, and localizes to early endosomes despite th
23 re evolutionarily related, and establish the nephrocyte as a simple model in which to study podocyte
26 on of APOL1 risk variants in D. melanogaster nephrocytes caused cell-autonomous accumulation of the e
29 ph by uptake of molecules through an SD-like nephrocyte diaphragm (ND) into labyrinthine channels tha
30 structure revealed that the formation of the nephrocyte diaphragm and lacunar structure, which is ess
37 xpression of the APOL1 G0 or G1 transgene in nephrocytes, fly cells homologous to mammalian podocytes
39 As transgenic flies with either allele aged, nephrocyte function declined, cell size increased, and n
40 ion of an APOL1 transgene initially enhances nephrocyte function, causing hypertrophy and subsequent
43 cells and oenocytes (also called Drosophila nephrocytes) function in taking up waste material from t
44 lencing Cindr in nephrocytes led to dramatic nephrocyte functional impairment and shortened life span
45 und that 85% of these genes are required for nephrocyte functions, suggesting that a majority of huma
46 co-expressed within binucleate garland cell nephrocytes (GCNs) that contribute to detoxification of
49 data suggest that the Drosophila pericardial nephrocyte is a useful in vivo model to help identify ge
50 shortened life span, as well as collapse of nephrocyte lacunar channels and effacement of nephrocyte
54 te, but the lack of a functional readout for nephrocytes makes it challenging to study this model of
61 d fluorescent protein and combined it with a nephrocyte-specific driver for targeted gene knockdown,
62 ulation was found at garland and pericardial nephrocytes supporting its role in organismal defence an
63 ch are pairs of highly endocytic pericardial nephrocytes that modulate cardiac function by uncharacte
65 bsorption is required for the maintenance of nephrocyte ultrastructure and fly survival under conditi
66 rgeted expression of human AMN in Drosophila nephrocytes was sufficient to rescue defective protein u
67 Using RNAi and conditional CRISPR/Cas9 in nephrocytes, we found this pattern depends on the expres
68 pression of dCubilin and dAMN is specific to nephrocytes, where they function as co-receptors for pro
69 ctional genetic screen of Drosophila cardiac nephrocytes, which are equivalents of mammalian podocyte
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