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NBAS encodes a protein with two leucine zipper domains, a ribosomal protein S14 signature domain and a Sec39 like domain.
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NBAS mutations cause a multisystem disorder involving bone, connective tissue, liver, immune system, and retina.
Biallelic Mutations in NBAS Cause Recurrent Acute Liver Failure with Onset in Infancy.
Data indicate that expression of several predicted chimeric genes and genes with disrupted exon structure including ALK (show ALK Antibodies), NBAS, FHIT, PTPRD (show PTPRD Antibodies) and ODZ4 in neuroblastoma (show ARHGEF16 Antibodies).
DHX34 (show DHX34 Antibodies) and NBAS act in concert with core nonsense-mediated mRNA decay factors to co-regulate a large number of endogenous RNA targets.
These findings suggest that function of NBAS may associate with the pathogenesis of short stature syndrome as well as optic atrophy and Pelger-Huet anomaly.
There may be a subset of NB in which enhanced DDX1 (show DDX1 Antibodies) and low-NAG (show NAGLU Antibodies) expression consequent to DDX1 (show DDX1 Antibodies) co-amplification without NAG (show NAGLU Antibodies) amplification contributes to susceptibility to intensive therapy.
Results together suggest that NAG (show NAGLU Antibodies) links between p31 (show ATP6V1E1 Antibodies) and ZW10 (show ZW10 Antibodies)-RINT-1 (show RINT1 Antibodies) and is involved in Golgi-to-ER transport.
Defects in NAG (show NAGLU Antibodies)-ELMO1 (show ELMO1 Antibodies) is associated with leukemic progression.
This gene encodes a protein with two leucine zipper domains, a ribosomal protein S14 signature domain and a Sec39 like domain. The protein is thought to be involved in Golgi-to-ER transport. Mutations in this gene are associated with short stature, optic nerve atrophy, and Pelger-Huet anomaly.
, neuroblastoma amplified sequence
, neuroblastoma-amplified protein
, neuroblastoma-amplified sequence
, neuroblastoma-amplified sequence-like
, NAG/BC035112 fusion
, NAG/FAM49A fusion
, neuroblastoma-amplified gene protein