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POLR3B encodes the second largest subunit of RNA polymerase III, the polymerase responsible for synthesizing transfer and small ribosomal RNAs in eukaryotes. Additionally we are shipping Polymerase (RNA) III (DNA Directed) Polypeptide B Proteins (3) and many more products for this protein.
Showing 10 out of 43 products:
Human Monoclonal POLR3B Primary Antibody for ELISA, WB - ABIN527631
Shen, Lei, Liu, Zheng, Song, Marc, Wang, Sun, Liang: Identification and characterization of INMAP, a novel interphase nucleus and mitotic apparatus protein that is involved in spindle formation and cell cycle progression. in Experimental cell research 2009
Cow (Bovine) Polyclonal POLR3B Primary Antibody for WB - ABIN2783516
Yee, Gong, Huang, Lorent, Dolan, Maraia, Pack: Mutation of RNA Pol III subunit rpc2/polr3b Leads to Deficiency of Subunit Rpc11 and disrupts zebrafish digestive development. in PLoS biology 2007
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 (show POLR3A Antibodies) and POLR3B without the classic MRI (show C7ORF49 Antibodies) 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 (show C7ORF49 Antibodies) presentation of POLR3-related disorders
first reports of long deletions causing POLR3-related leukodystrophy, suggesting that deletions and duplications in POLR3A (show POLR3A Antibodies) or POLR3B should be investigated in patients with a compatible phenotype
Mutations in POLR3A (show POLR3A Antibodies) or POLR3B are rare in patients with unclassified hypomyelination.
INMAP as a model regulator of CENP-B (show CENPB Antibodies)
These results suggest that INMAP might function through p53 (show TP53 Antibodies)/p21 (show CDKN1A Antibodies) pathways.
Most patients with 4H leukodystrophy carried the common c.1568T>A POLR3B mutation on one allele.
MRI (show C7ORF49 Antibodies) in patients with POLR3B mutations revealed smaller cerebellar structures, especially vermis, than those in POLR3A (show POLR3A Antibodies) mutations. MRI (show C7ORF49 Antibodies) also showed milder hypomyelination in patients with POLR3B mutations than those with POLR3A (show POLR3A Antibodies) mutations
Investigated POLR3A (show POLR3A Antibodies) and POLR3B mutations in patients with genetically unexplained hypomyelinating leukodystrophies with features of Pol III-related leukodystrophies. Recessive mutations in POLR3A (show POLR3A Antibodies) or POLR3B were uncovered in all 14 patients.
The Polr3b in the hippocampus in the prefrontal cortex of the DBA (show RPS19 Antibodies)/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