ARID3A Lentiviral Vector (Human) (CMV) (pLenti-GIII-CMV-RFP-2A-Puro)

Product name : ARID3A Lentiviral Vector (Human) (CMV) (pLenti-GIII-CMV-RFP-2A-Puro)

Catalog number : LV079993

Supplier : ABM lentivectors

Price : 322.5 EUR

Size : 1.0 µg DNA

More about:

Classification : AT-rich interaction domain containing

Concept : Scope note: The transfer of bacterial DNA by phages from an infected bacterium to another bacterium. This also refers to the transfer of genes into eukaryotic cells by viruses. This naturally occurring process is routinely employed as a GENE TRANSFER TECHNIQUE.

Discovery year : 1997-08-22

Entrez Gene : AT-rich interaction domain 3A  (ARID3A)  (NBN)

Entrez gene record : 1820

GenBank acession : U88047

Gene : ARID3A

Gene ontology - Biological process : positive regulation of transcription from RNA polymerase II promoter transcription from RNA polymerase II promoter DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest

Gene ontology - Cellular component : nucleus cytosol nucleoplasm intracellular membrane-bounded organelle membrane raft

Gene ontology - Molecular function : protein binding RNA polymerase II regulatory region sequence-specific DNA binding protein homodimerization activity chromatin binding transcriptional activator activity, RNA polymerase II transcription regulatory region sequence-specific binding

Havana BLAST/BLAT : OTTHUMG00000182018

Identity : 3031

InterPro : ARID DNA-binding domain  (HLA-DOA) REKLES domain

Locus : 19p13.3

Long gene name : AT-rich interaction domain 3A

Name : Transduction, Genetic

PubMed : Clinical trial of gene-disease association and gene-environment interaction. (HuGE Navigator) These results indicate both cooperative and interdependent roles for ARID3A and p53 in the transcriptional activation of p21(WAF1) in response to DNA damage. a putative p53-binding site was found, which specifically responded to p53, in the second intron of the E2FBP1/DRIL1 gene Bright is not expressed in all human B lymphocyte subpopulations. identify Bright as a contributor to accessibility of the IgH enhancer Solution NMR structure of the ARID domain of human ARID3A. Bright/ARID3a inhibition causes increased developmental plasticity in mouse and human cells. functions as a critical antagonist to the p16(INK4A)-Rb tumor suppressor machinery by regulating promyelocytic leukemia protein stability Systemic lupus erythematosus (SLE) patients had increased ARID3a B cells compared to healthy controls. ARID3a was not expressed in naive B cells of controls, but was abundant in SLE patients. Number of ARID3a B cells correlated with disease activity. These data reveal new functions for ARID3a in early hematopoiesis and suggest that knowledge regarding ARID3a levels in HSPCs could be informative for applications requiring transplantation of those cells.

Pubmed identfication : 9722953

Qualifiers : classification, economics, history, instrumentation, methods, standards, trends, utilization, veterinary, statistics & numerical data, ethics

RefSeq identity : NM_005224

Synonyms : BRIGHT

Synonyms gene : DRIL1

Synonyms gene name : dead ringer-like 1 (Drosophila) AT rich interactive domain 3A (BRIGHT- like) AT rich interactive domain 3A (BRIGHT-like)

Tree numbers : E05.393.350.800

WikiPathWays : TP53 Regulates Transcription of Cell Cycle Genes