Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Ribosomes, the organelles that catalyze protein synthesis, consist of a small 40S subunit and a large 60S subunit. Additionally we are shipping RPS19 Proteins (23) and RPS19 Kits (14) and many more products for this protein.
Showing 10 out of 96 products:
Human Monoclonal RPS19 Primary Antibody for ELISA, WB - ABIN562734
Rey, Duffy, Brown, Kennedy, Dick, Dror, Tailor: Enhanced alternative splicing of the FLVCR1 gene in Diamond Blackfan anemia disrupts FLVCR1 expression and function that are critical for erythropoiesis. in Haematologica 2008
Show all 5 references for ABIN562734
Human Polyclonal RPS19 Primary Antibody for EIA, WB - ABIN954614
Devlin, Dacosta, Mohandas, Elliott, Bodine: A transgenic mouse model demonstrates a dominant negative effect of a point mutation in the RPS19 gene associated with Diamond-Blackfan anemia. in Blood 2010
Show all 5 references for ABIN954614
Human Polyclonal RPS19 Primary Antibody for ELISA, WB - ABIN185519
Léger-Silvestre, Caffrey, Dawaliby, Alvarez-Arias, Gas, Bertolone, Gleizes, Ellis: Specific Role for Yeast Homologs of the Diamond Blackfan Anemia-associated Rps19 Protein in Ribosome Synthesis. in The Journal of biological chemistry 2005
RPS19-downregulated erythroleukemia cells show reduced FLVCR1a and FLVCR1b mRNA levels associated with heme overload.
Loss of RPS19 expression is associated with Diamond-Blackfan anemia.
Mutations R62W and R101H impair RPS19 ability to associate with the ribosome.
Data indicate that GATA1 (show GATA1 Antibodies) transcription factor is downregulated in ribosomal protein S19 (RPS19)-deficient cells through upregulation of TNF-alpha (show TNF Antibodies) and p38 MAPK (show MAPK14 Antibodies).
RPS19 mutation is associated with Diamond Blackfan Anemia.
A binding domain for RPS19 was identified and characterized in the N-terminus.
increase of autophagy in cells derived from DBA patients, in CD34 (show CD34 Antibodies)+ erythrocyte progenitor cells with RPS19 knock down, in the red blood cells of zebrafish embryos with RP-deficiency, and in cells from patients with Shwachman-Diamond syndrome
levels of branched-chain aminotransferase-1 (BCAT1 (show BCAT1 Antibodies)) transcripts are significantly decreased on the polysomes of both RPS19 and RPL11 (show RPL11 Antibodies) cells and that translation of BCAT1 (show BCAT1 Antibodies) protein is especially impaired in cells with small RP gene mutations
High frequency of RPS19 gene deletion is associated with Italian Diamond-Blackfan anemia.
RPS19 mutations induced a decrease in proliferation of progenitor cells, but the terminal erythroid differentiation was normal with little or no apoptosis.
indicate the importance of the RP S19 (show ASAP1 Antibodies) oligomer-induced macrophage recruitment in coagulum resorption
Rps19 mutant embryonic stem cells showed significant increase in p53 (show TP53 Antibodies) protein expression.
We report the generation of mouse models for RPS19-deficient Diamond Blackfan anemia using transgenic RNA interference that allows an inducible and graded down-regulation of Rps19.
generated a transgenic model expressing an RPS19 mutation in which an arginine residue is replaced with a tryptophan residue at codon 62 as a model of Diamond-Blackfan anemia
Combined Rps19 insufficiency and Pim-1 (show PIM1 Antibodies) deficiency promote murine myeloid cell growth through a deregulation of c-Myc (show MYC Antibodies) and a simultaneous up-regulation of anti-apoptotic Bcl proteins.
RPS19 mRNA and protein expression were shown to decrease during terminal erythroid differentiation.
Results indicate that ribosomal protein S19 (-/-) zygotes do not form blastocysts, whereas one normal Rps19 allele in mice is sufficient to maintain normal ribosomal and possibly extraribosomal functions.
presence of an RP S19 (show ASAP1 Antibodies) dimer- and C5a receptor-mediated autocrine-type augmentation mechanism during Mn II-induced apoptosis in the mouse fibroblastic cell line
the loss of one Rps19 allele in mice is fully compensated for at the transcriptional level with preservation of erythropoiesis
Study reports two mouse dark skin (Dsk) loci caused by mutations in Rps19 (ribosomal protein S19) and Rps20 (ribosomal protein S20 (show RPS20 Antibodies)).
Ribosomes, the organelles that catalyze protein synthesis, consist of a small 40S subunit and a large 60S subunit. Together these subunits are composed of 4 RNA species and approximately 80 structurally distinct proteins. This gene encodes a ribosomal protein that is a component of the 40S subunit. The protein belongs to the S19E family of ribosomal proteins. It is located in the cytoplasm. Mutations in this gene cause Diamond-Blackfan anemia (DBA), a constitutional erythroblastopenia characterized by absent or decreased erythroid precursors, in a subset of patients. This suggests a possible extra-ribosomal function for this gene in erythropoietic differentiation and proliferation, in addition to its ribosomal function. Higher expression levels of this gene in some primary colon carcinomas compared to matched normal colon tissues has been observed. As is typical for genes encoding ribosomal proteins, there are multiple processed pseudogenes of this gene dispersed through the genome.
ribosomal protein S19
, 40S ribosomal protein S19