Anti-FKHRL1

Anti-FKHRL1
Item number Size Datasheet Manual SDS Delivery time Quantity Price
ELK-ES8898.50 50 µl - -

10 - 14 business days*

173.00€
ELK-ES8898.100 100 µl - -

10 - 14 business days*

290.00€
 
This gene belongs to the forkhead family of transcription factors which are characterized by a... more
Product information "Anti-FKHRL1"
This gene belongs to the forkhead family of transcription factors which are characterized by a distinct forkhead domain. This gene likely functions as a trigger for apoptosis through expression of genes necessary for cell death. Translocation of this gene with the MLL gene is associated with secondary acute leukemia. Alternatively spliced transcript variants encoding the same protein have been observed. [provided by RefSeq, Jul 2008], Protein function: Transcriptional activator that recognizes and binds to the DNA sequence 5'-[AG]TAAA[TC]A-3' and regulates different processes, such as apoptosis and autophagy (PubMed:10102273, PubMed:16751106, PubMed:21329882, PubMed:30513302). Acts as a positive regulator of autophagy in skeletal muscle: in starved cells, enters the nucleus following dephosphorylation and binds the promoters of autophagy genes, such as GABARAP1L, MAP1LC3B and ATG12, thereby activating their expression, resulting in proteolysis of skeletal muscle proteins. Triggers apoptosis in the absence of survival factors, including neuronal cell death upon oxidative stress (PubMed:10102273, PubMed:16751106). Participates in post-transcriptional regulation of MYC: following phosphorylation by MAPKAPK5, promotes induction of miR- 34b and miR-34c expression, 2 post-transcriptional regulators of MYC that bind to the 3'UTR of MYC transcript and prevent its translation (PubMed:21329882). In response to metabolic stress, translocates into the mitochondria where it promotes mtDNA transcription (PubMed:23283301). In response to metabolic stress, translocates into the mitochondria where it promotes mtDNA transcription. Also acts as a key regulator of chondrogenic commitment of skeletal progenitor cells in response to lipid availability: when lipids levels are low, translocates to the nucleus and promotes expression of SOX9, which induces chondrogenic commitment and suppresses fatty acid oxidation. Also acts as a key regulator of regulatory T-cells (Treg) differentiation by activating expression of FOXP3 (PubMed:30513302). [The UniProt Consortium] Recommended dilutions: WB 1:500-2000, ELISA 1:10000-20000. Cellular localization: Cytoplasm, cytosol . Nucleus . Mitochondrion matrix . Mitochondrion outer membrane , Peripheral membrane protein , Cytoplasmic side . Retention in the cytoplasm contributes to its inactivation (PubMed:10102273, PubMed:15084260, PubMed:16751106). Translocates to the nucleus upon oxidative stress and in the absence of survival factors (PubMed:10102273, PubMed:16751106). Translocates from the cytosol to the nucleus following dephosphorylation in response to autophagy-inducing stimuli (By similarity). Translocates in a AMPK-dependent manner into the mitochondrion in response to metabolic stress (PubMed:23283301, PubMed:29445193). Serum deprivation increases localization to the nucleus, leading to activate expression of SOX9 and subsequent chondrogenesis (By similarity). .
Keywords: Anti-AF6q21 protein, Anti-Forkhead box protein O3, Anti-Forkhead in rhabdomyosarcoma-like 1, FKHRL1 rabbit pAb
Supplier: ELK Biotechnology
Supplier-Nr: ES8898

Properties

Application: WB, ELISA
Antibody Type: Polyclonal
Conjugate: No
Host: Rabbit
Species reactivity: human, mouse, rat
Immunogen: Synthesized peptide derived from human FKHRL1 Polyclonal
MW: 65 kD
Format: Purified

Handling & Safety

Storage: -20°C
Shipping: +4°C (International: +4°C)
Caution
Our products are for laboratory research use only: Not for administration to humans!
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