hnRNP A2B1 Antibody [A10M11] | Primary Antibodies

Application: Reactivity: Rat, Mouse, Human

Usage Information

Dilution
WB1:1000 IHC1:5000 IF1:1000 FCM1:500

Application
WB, IHC, IF, FCM

Reactivity
Rat, Mouse, Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
37 kDa 38 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
hnRNP A2B1 Antibody [A10M11] detects endogenous levels of total hnRNP A2B1 protein.

Clone
A10M11

Synonym(s)
HNRPA2B1, HNRNPA2B1, Heterogeneous nuclear ribonucleoproteins A2/B1, hnRNP A2/B1

Background
hnRNP A2B1, a member of the heterogeneous nuclear ribonucleoprotein family, functions as a versatile RNA-binding protein that shuttles between nucleus and cytoplasm to orchestrate pre-mRNA processing and mRNA transport. It consists of two N-terminal RNA recognition motifs (RRMs) for sequence-specific binding to A2 response elements (A2REs) on target transcripts and a glycine-rich C-terminal domain that mediates protein-protein interactions and phase separation into membraneless organelles. In RNA metabolism, hnRNP A2B1 binds nascent pre-mRNAs to regulate alternative splicing of cell proliferation genes like RON and CD44 by competing with U2AF65 at polypyrimidine tracts, while also packaging mature mRNAs into RNP granules for nuclear export and dendritic localization in neurons. The protein activates STAT3 and ERK1/2 signaling through splicing of oncogenic isoforms that encode cytoplasmic variants with enhanced signaling potential, promoting epithelial-mesenchymal transition and invasion in breast cancer cells. In tauopathies, hnRNP A2B1 forms a pathological complex with oligomeric tau and N6-methyladenosine (m6A)-marked RNAs, sequestering transcripts into stress granules that impair global translation and trigger integrated stress response via eIF2α phosphorylation. hnRNP A2B1 directs transport of β-actin mRNA to neuronal growth cones via A2RE recognition, supporting synapse formation and plasticity. Knockdown disrupts m6A reader function, releases tau-induced translation block, and ameliorates neurodegeneration in P301S tau mice. Overexpression correlates with poor prognosis in breast cancer subtypes, while cytoplasmic mislocalization appears in Alzheimer's disease brains alongside tau aggregates.

Background

hnRNP A2B1, a member of the heterogeneous nuclear ribonucleoprotein family, functions as a versatile RNA-binding protein that shuttles between nucleus and cytoplasm to orchestrate pre-mRNA processing and mRNA transport. It consists of two N-terminal RNA recognition motifs (RRMs) for sequence-specific binding to A2 response elements (A2REs) on target transcripts and a glycine-rich C-terminal domain that mediates protein-protein interactions and phase separation into membraneless organelles. In RNA metabolism, hnRNP A2B1 binds nascent pre-mRNAs to regulate alternative splicing of cell proliferation genes like RON and CD44 by competing with U2AF65 at polypyrimidine tracts, while also packaging mature mRNAs into RNP granules for nuclear export and dendritic localization in neurons. The protein activates STAT3 and ERK1/2 signaling through splicing of oncogenic isoforms that encode cytoplasmic variants with enhanced signaling potential, promoting epithelial-mesenchymal transition and invasion in breast cancer cells. In tauopathies, hnRNP A2B1 forms a pathological complex with oligomeric tau and N6-methyladenosine (m6A)-marked RNAs, sequestering transcripts into stress granules that impair global translation and trigger integrated stress response via eIF2α phosphorylation. hnRNP A2B1 directs transport of β-actin mRNA to neuronal growth cones via A2RE recognition, supporting synapse formation and plasticity. Knockdown disrupts m6A reader function, releases tau-induced translation block, and ameliorates neurodegeneration in P301S tau mice. Overexpression correlates with poor prognosis in breast cancer subtypes, while cytoplasmic mislocalization appears in Alzheimer's disease brains alongside tau aggregates.

References
https://pubmed.ncbi.nlm.nih.gov/28351333/ https://pubmed.ncbi.nlm.nih.gov/32588964/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%