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Gene Information

Gene symbol: MYO1E

Gene name: myosin IE

HGNC ID: 7599

Synonyms: MYO1C, HuncM-IC, MGC104638

Related Genes

# Gene Symbol Number of hits
1 ACTN4 1 hits
2 COL4A5 1 hits
3 GDF15 1 hits
4 IMMT 1 hits
5 NEIL1 1 hits
6 NPHS1 1 hits
7 PARP1 1 hits
8 TGFA 1 hits
9 TJP1 1 hits

Related Sentences

# PMID Sentence
1 21697813 Exome sequencing identified MYO1E and NEIL1 as candidate genes for human autosomal recessive steroid-resistant nephrotic syndrome.
2 21697813 Exome sequencing identified two homozygous missense variants within the chromosome 15 segment; an A159P substitution in myosin 1E (MYO1E), encoding a podocyte cytoskeletal protein; and an E181K substitution in nei endonuclease VIII-like 1 (NEIL1), encoding a base-excision DNA repair enzyme.
3 21697813 Screening 71 additional patients with SRNS, however, did not identify independent NEIL1 or MYO1E mutations, suggesting larger sequencing efforts are needed to uncover which mutation is responsible for the phenotype.
4 21697813 Exome sequencing identified MYO1E and NEIL1 as candidate genes for human autosomal recessive steroid-resistant nephrotic syndrome.
5 21697813 Exome sequencing identified two homozygous missense variants within the chromosome 15 segment; an A159P substitution in myosin 1E (MYO1E), encoding a podocyte cytoskeletal protein; and an E181K substitution in nei endonuclease VIII-like 1 (NEIL1), encoding a base-excision DNA repair enzyme.
6 21697813 Screening 71 additional patients with SRNS, however, did not identify independent NEIL1 or MYO1E mutations, suggesting larger sequencing efforts are needed to uncover which mutation is responsible for the phenotype.
7 21697813 Exome sequencing identified MYO1E and NEIL1 as candidate genes for human autosomal recessive steroid-resistant nephrotic syndrome.
8 21697813 Exome sequencing identified two homozygous missense variants within the chromosome 15 segment; an A159P substitution in myosin 1E (MYO1E), encoding a podocyte cytoskeletal protein; and an E181K substitution in nei endonuclease VIII-like 1 (NEIL1), encoding a base-excision DNA repair enzyme.
9 21697813 Screening 71 additional patients with SRNS, however, did not identify independent NEIL1 or MYO1E mutations, suggesting larger sequencing efforts are needed to uncover which mutation is responsible for the phenotype.
10 23715127 Myo1c is a non-muscle myosin motor protein that interacts directly with nephrin and neph1, and mediates their intracellular transport to the podocyte intercellular junction.
11 23761676 Myo1e-null podocytes expressing FSGS-associated myo1e mutant (A159P) did not efficiently assemble actin cables along new cell-cell junctions.
12 23761676 We have mapped domains in myo1e that were critical for its localization to cell-cell junctions and determined that the SH3 domain of myo1e tail interacts with ZO-1, a component of the slit diaphragm complex and tight junctions.
13 23761676 Myo1e-null podocytes expressing FSGS-associated myo1e mutant (A159P) did not efficiently assemble actin cables along new cell-cell junctions.
14 23761676 We have mapped domains in myo1e that were critical for its localization to cell-cell junctions and determined that the SH3 domain of myo1e tail interacts with ZO-1, a component of the slit diaphragm complex and tight junctions.
15 25739341 Coinheritance of COL4A5 and MYO1E mutations accentuate the severity of kidney disease.
16 31097328 The motor protein Myo1c regulates transforming growth factor-β-signaling and fibrosis in podocytes.
17 31097328 Differential expression analysis of nuclear Myo1c-associated gene promoters showed that nuclear Myo1c targeted the TGF-β responsive gene growth differentiation factor (GDF)-15 and directly bound to the GDF-15 promoter.
18 31097328 The motor protein Myo1c regulates transforming growth factor-β-signaling and fibrosis in podocytes.
19 31097328 Differential expression analysis of nuclear Myo1c-associated gene promoters showed that nuclear Myo1c targeted the TGF-β responsive gene growth differentiation factor (GDF)-15 and directly bound to the GDF-15 promoter.