产品名称
Anti-hnRNP-A1 antibody, Mouse monoclonal, ~2 mg/mL, clone 4B10, purified from hybridoma cell culture
biological source
mouse
conjugate
unconjugated
antibody form
purified from hybridoma cell culture
antibody product type
primary antibodies
clone
4B10, monoclonal
form
buffered aqueous solution
mol wt
antigen 32-35 kDa
species reactivity
bovine, human, canine
concentration
~2 mg/mL
technique(s)
immunocytochemistry: suitable
immunoprecipitation (IP): suitable
indirect ELISA: suitable
microarray: suitable
western blot: 0.25-0.5 μg/mL using total cell extract of HeLa cells
isotype
IgG2a
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Quality Level
Gene Information
human ... HNRNPA1(3178)
Application
Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Western Blotting (1 paper)
Western Blotting (1 paper)
Monoclonal Anti-hnRNP-A1 antibody produced in mouse has also been used in:
- enzyme linked immunosorbent assay (ELISA)
- immunoblotting
- immunoprecipitation
- immunocytochemistry.
Biochem/physiol Actions
Heterogeneous nuclear ribonucleoprotein A1 (hnRNP-A1) is important in biological activities such as transcription, pre-mRNA processing, cytoplasmic mRNA translation and turnover. hnRNP-A1 is important in pre-mRNA processing and in mRNA export from the nucleus. The protein contains a 38-amino acid domain called M9, which is important for the interaction with the transportin protein and therefore, for its import and export from the nucleus. RanGTP mediates dissociation of hnRNP-A1 from transportin. Higher expression is observed in proliferating and/or transformed cells than in differentiated tissues.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
General description
Monoclonal Anti-hnRNP-A1 (mouse IgG2a isotype) is derived from the 4B10 hybridoma produced by the fusion of mouse myeloma cells (SP2/0 cells) and splenocytes from NZB mice immunized with purified human hnRNPA1. Heterogeneous nuclear ribonucleoprotein A1 (hnRNPs) consist of protein groups named A to U and many of these protein groups consist of more than one isoform. The major steady-state proteins of the isolated hnRNP complex are A1, A2, B1, B2, C1, and C2, with a range of molecular weight starting with 34 kDa up to 43 kDa. hnRNP-A1 is ubiquitously expressed in cells and tissues.
Immunogen
purified human hnRNP-A1.
Physical form
Solution in 0.01 M phosohate buffered saline, pH 7.4, and 15 mM sodium azide.
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存储类别
10 - Combustible liquids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
法规信息
常规特殊物品
此项目有
Functional diversity of the hnRNPs: past, present and perspectives
Han SP, et al.
The Biochemical Journal, 430(3), 379-392 (2010)
hnRNP A1 nucleocytoplasmic shuttling activity is required for normal myelopoiesis and BCR/ABL leukemogenesis
Lervolino A, et al.
Molecular and Cellular Biology, 22(7), 2255-2266 (2002)
Blocking of an intronic splicing silencer completely rescues IKBKAP exon 20 splicing in familial dysautonomia patient cells
Bruun GH, et al.
Nucleic Acids Research, 46(15), 7938-7952 (2018)
Youn-Jae Kim et al.
PloS one, 6(12), e28308-e28308 (2011-12-14)
Aberrant miR-21 expression is closely associated with cell proliferation, anti-apoptosis, migration, invasion, and metastasis in various cancers. However, the regulatory mechanism of miR-21 biogenesis is largely unknown. Here, we demonstrated that the tumor suppressor PTEN negatively regulates the expression of
Gitte H Bruun et al.
Nucleic acids research, 46(15), 7938-7952 (2018-05-16)
Familial dysautonomia (FD) is a severe genetic disorder causing sensory and autonomic dysfunction. It is predominantly caused by a c.2204+6T>C mutation in the IKBKAP gene. This mutation decreases the 5' splice site strength of IKBKAP exon 20 leading to exon
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