|Institutional Source||Beutler Lab|
|Gene Name||myosin, heavy polypeptide 10, non-muscle|
|Synonyms||Myosin IIB, Fltn, Fltn, Myhn-2, myosin IIB, nonmuscle myosin heavy chain II-B, NMHC-B, Myhn2, SMemb, NMHC II-B, 5730504C04Rik, nonmuscle myosin heavy chain IIB, 9330167F11Rik|
|Is this an essential gene?||Essential (E-score: 1.000)|
|Stock #||R4666 (G1)|
|Chromosomal Location||68691559-68816632 bp(+) (GRCm38)|
|Type of Mutation||critical splice donor site (1 bp from exon)|
|DNA Base Change (assembly)||G to A at 68801730 bp (GRCm38)|
|Amino Acid Change|
|Ref Sequence||ENSEMBL: ENSMUSP00000099671 (fasta)|
|Gene Model||predicted gene model for transcript(s): [ENSMUST00000018887] [ENSMUST00000092984] [ENSMUST00000102611]|
|Coding Region Coverage||
FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a member of the myosin superfamily. The protein represents a conventional non-muscle myosin; it should not be confused with the unconventional myosin-10 (MYO10). Myosins are actin-dependent motor proteins with diverse functions including regulation of cytokinesis, cell motility, and cell polarity. Mutations in this gene have been associated with May-Hegglin anomaly and developmental defects in brain and heart. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Dec 2011]
PHENOTYPE: Nullizygous mice show pre- and neonatal death, heart defects and hydrocephaly. Deletion of exon B1 disrupts migration of facial neurons, whereas deletion of exon B2 leads to Purkinje cell anomalies. Hypomorphs show hydrocephaly and defects in motor control, cerebellar foliation and neuron migration. [provided by MGI curators]
|Allele List at MGI|
|Other mutations in this stock||
|Other mutations in Myh10||
(F):5'- GTCTGCTGCAGGTAACCTAG -3'
(R):5'- ATGAAGCCACGCTCTGTCTG -3'
(F):5'- TGCTGCAGGTAACCTAGACACC -3'
(R):5'- AAGCCACGCTCTGTCTGTAAGG -3'