Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
POLR3B encodes the second largest subunit of RNA polymerase III, the polymerase responsible for synthesizing transfer and small ribosomal RNAs in eukaryotes. De plus, nous expédions Polymerase (RNA) III (DNA Directed) Polypeptide B Anticorps (51) et et beaucoup plus de produits pour cette protéine.
Showing 3 out of 3 products:
Novel compound heterozygous variations in POLR3B were identified in a patient with cerebellar hypoplasia with endosteal sclerosis.
The spectrum of phenotypes resulting from POLR3B mutations is wider than previously believed.
Findings suggest that AP-1 factors are regulators of RNA polymerase III (Pol III)-driven 5S rRNA and U6 snRNA expression with a potential role in cell proliferation.
Multicenter retrospective study to collect neuroradiologic, clinical, and molecular data of patients with mutations in POLR3A and POLR3B without the classic MRI phenotype: diffuse hypomyelination is not an obligatory feature of POLR3-related disorders; two distinct patterns, selective involvement of the corticospinal tracts and cerebellar atrophy, are added to the MRI presentation of POLR3-related disorders
first reports of long deletions causing POLR3-related leukodystrophy, suggesting that deletions and duplications in POLR3A or POLR3B should be investigated in patients with a compatible phenotype
Mutations in POLR3A or POLR3B are rare in patients with unclassified hypomyelination.
INMAP as a model regulator of CENP-B
These results suggest that INMAP might function through p53/p21 pathways.
Most patients with 4H leukodystrophy carried the common c.1568T>A POLR3B mutation on one allele.
MRI in patients with POLR3B mutations revealed smaller cerebellar structures, especially vermis, than those in POLR3A mutations. MRI also showed milder hypomyelination in patients with POLR3B mutations than those with POLR3A mutations
Investigated POLR3A and POLR3B mutations in patients with genetically unexplained hypomyelinating leukodystrophies with features of Pol III-related leukodystrophies. Recessive mutations in POLR3A or POLR3B were uncovered in all 14 patients.
study reports INMAP is a truncated version of POLR3B, and is up-regulated in several human cancer cell lines; results suggest that INMAP may function through the p53 and AP-1 pathways, providing a possible link of its activity with tumourigenesis
Mutations in POLR3A and POLR3B encoding RNA Polymerase III subunits cause an autosomal-recessive hypomyelinating leukoencephalopathy
Recessive mutations in POLR3B, encoding the second largest subunit of Pol III, cause a rare hypomyelinating leukodystrophy
Results suggest that INMAP is a novel protein that plays essential role in spindle formation and cell-cycle progression.
Data describe the purification and identification of RNA polymerase III subunits RPC2 and RPC5.
The Polr3b in the hippocampus in the prefrontal cortex of the DBA/2 J strain were up-regulated.
This gene encodes the second largest subunit of RNA polymerase III, the polymerase responsible for synthesizing transfer and small ribosomal RNAs in eukaryotes. The largest subunit and the encoded protein form the catalytic center of RNA polymerase III. Mutations in this gene are a cause of hypomyelinating leukodystrophy. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
DNA-directed RNA polymerase III subunit RPC2
, DNA-directed RNA polymerase III 127.6 kDa polypeptide
, DNA-directed RNA polymerase III subunit B
, RNA polymerase III subunit C2
, DNA-directed RNA polymerase III B
, RNA polymerase III subunit RPC2 homolog