Mouse Anti-TIA1 Recombinant Antibody (CBYJT-3102) (CBMAB-T2369-YJ)

Mouse

Human

CBYJT-3102

IgG1

IHC-Fr, IHC-P

Human

IgG1

Monoclonal

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

PBS, pH 7.5, BSA

0.02% Sodium Azide

Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

TIA1 Cytotoxic Granule Associated RNA Binding Protein

TIA1 is a member of a RNA-binding protein family and possesses nucleolytic activity against cytotoxic lymphocyte (CTL) target cells. It has been suggested that this protein may be involved in the induction of apoptosis as it preferentially recognizes poly(A) homopolymers and induces DNA fragmentation in CTL targets. The major granule-associated species is a 15-kDa protein that is thought to be derived from the carboxyl terminus of the 40-kDa product by proteolytic processing.

TIA1 Cytotoxic Granule Associated RNA Binding Protein; T-Cell-Restricted Intracellular Antigen-1; Nucleolysin TIA-1 Isoform P40; TIA-1; TIA1 Cytotoxic Granule-Associated RNA-Binding Protein; P40-TIA-1 (Containing P15-TIA-1)

RNA-binding protein involved in the regulation of alternative pre-RNA splicing and mRNA translation by binding to uridine-rich (U-rich) RNA sequences (PubMed:8576255, PubMed:11106748, PubMed:12486009, PubMed:17488725).
Binds to U-rich sequences immediately downstream from a 5' splice sites in a uridine-rich small nuclear ribonucleoprotein (U snRNP)-dependent fashion, thereby modulating alternative pre-RNA splicing (PubMed:11106748, PubMed:8576255).
Preferably binds to the U-rich IAS1 sequence in a U1 snRNP-dependent manner; this binding is optimal if a 5' splice site is adjacent to IAS1 (By similarity).
Activates the use of heterologous 5' splice sites; the activation depends on the intron sequence downstream from the 5' splice site, with a preference for a downstream U-rich sequence (PubMed:11106748).
By interacting with SNRPC/U1-C, promotes recruitment and binding of spliceosomal U1 snRNP to 5' splice sites followed by U-rich sequences, thereby facilitating atypical 5' splice site recognition by U1 snRNP (PubMed:11106748, PubMed:12486009, PubMed:17488725).
Activates splicing of alternative exons with weak 5' splice sites followed by a U-rich stretch on its own pre-mRNA and on TIAR mRNA (By similarity).
Acts as a modulator of alternative splicing for the apoptotic FAS receptor, thereby promoting apoptosis (PubMed:11106748, PubMed:1934064, PubMed:17488725).
Binds to the 5' splice site region of FAS intron 5 to promote accumulation of transcripts that include exon 6 at the expense of transcripts in which exon 6 is skipped, thereby leading to the transcription of a membrane-bound apoptotic FAS receptor, which promotes apoptosis (PubMed:11106748, PubMed:1934064, PubMed:17488725).
Binds to a conserved AU-rich cis element in COL2A1 intron 2 and modulates alternative splicing of COL2A1 exon 2 (PubMed:17580305).
Also binds to the equivalent AT-rich element in COL2A1 genomic DNA, and may thereby be involved in the regulation of transcription (PubMed:17580305).
Binds specifically to a polypyrimidine-rich controlling element (PCE) located between the weak 5' splice site and the intronic splicing silencer of CFTR mRNA to promote exon 9 inclusion, thereby antagonizing PTB1 and its role in exon skipping of CFTR exon 9 (PubMed:14966131).
Involved in the repression of mRNA translation by binding to AU-rich elements (AREs) located in mRNA 3' untranslated regions (3' UTRs), including target ARE-bearing mRNAs encoding TNF and PTGS2 (By similarity).
Also participates in the cellular response to environmental stress, by acting downstream of the stress-induced phosphorylation of EIF2S1/EIF2A to promote the recruitment of untranslated mRNAs to cytoplasmic stress granules (SGs), leading to stress-induced translational arrest (PubMed:10613902).
Formation and recruitment to SGs is regulated by Zn2+ (By similarity).
Possesses nucleolytic activity against cytotoxic lymphocyte target cells (PubMed:1934064).
Isoform Short
Displays enhanced splicing regulatory activity compared with TIA isoform Long.

Biological Process apoptotic processSource:ProtInc1 Publication
Biological Process mRNA processingSource:UniProtKB-KW
Biological Process negative regulation of cytokine productionSource:Ensembl
Biological Process negative regulation of translationSource:UniProtKB
Biological Process protein localization to cytoplasmic stress granuleSource:AgBase1 Publication
Biological Process regulation of alternative mRNA splicing, via spliceosomeSource:UniProtKB2 Publications
Biological Process regulation of mRNA splicing, via spliceosomeSource:UniProtKB2 Publications
Biological Process RNA splicingSource:UniProtKB-KW
Biological Process stress granule assemblySource:UniProtKB1 Publication

Nucleus
Cytoplasm
Cytoplasm, Stress granule
Accumulates in cytoplasmic stress granules (SG) following cellular damage (PubMed:15371533, PubMed:10613902).
Recruitment to SG is induced by Zn2+ (By similarity).

Welander distal myopathy (WDM):
An autosomal dominant disorder characterized by adult onset of distal muscle weakness predominantly affecting the distal long extensors of the hands, with slow progression to involve all small hand muscles and the lower legs. Skeletal muscle biopsy shows myopathic changes and prominent rimmed vacuoles. Rare homozygous patients showed earlier onset, faster progression, and proximal muscle involvement.
Amyotrophic lateral sclerosis 26, with or without frontotemporal dementia (ALS26):
A form of amyotrophic lateral sclerosis, a neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of the cases. ALS26 inheritance is autosomal dominant. Some patients may develop frontotemporal dementia.

Phosphorylated by FASTK; phosphorylation occurs after FAS ligation in FAS-mediated apoptosis and before DNA fragmentation.