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PMID |
Sentence |
1 |
15172686
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We detected many genes known to be important for metanephros development including Sall1, GDNF, Raldh2, Pax8 and FoxD1, and genes expressed abundantly in the metanephric mesenchyme such as Unc4.1, Six2, Osr-2 and PDGFc.
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2 |
15172686
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We also found groups of genes including SSB-4, Smarcd3, micro-Crystallin, TRB-2, which are not known to be expressed in the metanephric mesenchyme.
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3 |
26154924
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WT1 controls metanephric mesenchyme (MM) self-renewal and proliferation mainly by regulating FGF and BMP-pSMAD signaling pathways as well as Sall1 and Pax2, encoding key transcription factors; WT1 drives MM differentiation and mesenchyme-epithelial transition by targeting Fgf8 and Wnt4; WT1 defines podocyte identity by activation of other podocyte-specific transcription factors, including Mafb, Lmx1b, FoxC2, and Tcf21.
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4 |
26458176
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By recapitulating metanephric kidney development in vitro, we generate SIX2+ SALL1+ WT1+ PAX2+ NPCs with 90% efficiency within 9 days of differentiation.
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5 |
28759006
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To explore the significance of Sall1 in differentiated podocytes, we investigated podocyte-specific Sall1-deficient mice (Sall1 KOp°d°/p°d°) using a podocin-Cre/loxP system and siRNA Sall1 knockdown (Sall1 KD) podocytes.
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6 |
28759006
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Differentiated Sall1 KD podocytes showed a loss of synaptopodin, suppressed stress fiber formation, and, ultimately, impaired directed cell migration.
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7 |
28759006
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These results indicated that Sall1 has a protective role in podocytes; thus, we investigated the endoplasmic reticulum stress marker GRP78.
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8 |
28759006
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GRP78 expression was higher in ADR-treated Sall1 KOp°d°/p°d° mice than in control mice.
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9 |
28759006
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Sall1 appeared to influence the expression of GRP78 in injured podocytes.
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10 |
28759006
|
To explore the significance of Sall1 in differentiated podocytes, we investigated podocyte-specific Sall1-deficient mice (Sall1 KOp°d°/p°d°) using a podocin-Cre/loxP system and siRNA Sall1 knockdown (Sall1 KD) podocytes.
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11 |
28759006
|
Differentiated Sall1 KD podocytes showed a loss of synaptopodin, suppressed stress fiber formation, and, ultimately, impaired directed cell migration.
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12 |
28759006
|
These results indicated that Sall1 has a protective role in podocytes; thus, we investigated the endoplasmic reticulum stress marker GRP78.
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13 |
28759006
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GRP78 expression was higher in ADR-treated Sall1 KOp°d°/p°d° mice than in control mice.
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14 |
28759006
|
Sall1 appeared to influence the expression of GRP78 in injured podocytes.
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15 |
28759006
|
To explore the significance of Sall1 in differentiated podocytes, we investigated podocyte-specific Sall1-deficient mice (Sall1 KOp°d°/p°d°) using a podocin-Cre/loxP system and siRNA Sall1 knockdown (Sall1 KD) podocytes.
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16 |
28759006
|
Differentiated Sall1 KD podocytes showed a loss of synaptopodin, suppressed stress fiber formation, and, ultimately, impaired directed cell migration.
|
17 |
28759006
|
These results indicated that Sall1 has a protective role in podocytes; thus, we investigated the endoplasmic reticulum stress marker GRP78.
|
18 |
28759006
|
GRP78 expression was higher in ADR-treated Sall1 KOp°d°/p°d° mice than in control mice.
|
19 |
28759006
|
Sall1 appeared to influence the expression of GRP78 in injured podocytes.
|
20 |
28759006
|
To explore the significance of Sall1 in differentiated podocytes, we investigated podocyte-specific Sall1-deficient mice (Sall1 KOp°d°/p°d°) using a podocin-Cre/loxP system and siRNA Sall1 knockdown (Sall1 KD) podocytes.
|
21 |
28759006
|
Differentiated Sall1 KD podocytes showed a loss of synaptopodin, suppressed stress fiber formation, and, ultimately, impaired directed cell migration.
|
22 |
28759006
|
These results indicated that Sall1 has a protective role in podocytes; thus, we investigated the endoplasmic reticulum stress marker GRP78.
|
23 |
28759006
|
GRP78 expression was higher in ADR-treated Sall1 KOp°d°/p°d° mice than in control mice.
|
24 |
28759006
|
Sall1 appeared to influence the expression of GRP78 in injured podocytes.
|
25 |
28759006
|
To explore the significance of Sall1 in differentiated podocytes, we investigated podocyte-specific Sall1-deficient mice (Sall1 KOp°d°/p°d°) using a podocin-Cre/loxP system and siRNA Sall1 knockdown (Sall1 KD) podocytes.
|
26 |
28759006
|
Differentiated Sall1 KD podocytes showed a loss of synaptopodin, suppressed stress fiber formation, and, ultimately, impaired directed cell migration.
|
27 |
28759006
|
These results indicated that Sall1 has a protective role in podocytes; thus, we investigated the endoplasmic reticulum stress marker GRP78.
|
28 |
28759006
|
GRP78 expression was higher in ADR-treated Sall1 KOp°d°/p°d° mice than in control mice.
|
29 |
28759006
|
Sall1 appeared to influence the expression of GRP78 in injured podocytes.
|