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FKHRL1 rabbit pAb - ES8898FKHRL1 rabbit pAb Sizes: 50L, 100L Catalogue Numbers: ES8898 50, ES8898 100 Citations, Manuals and MSDS Available upon request. Background: 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
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FKHRL1 rabbit pAb

Sizes: 50μL, 100μL

Catalogue Numbers: ES8898-50, ES8898-100

Citations, Manuals and MSDS Available upon request.

Background: 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],

Alternate Name: Forkhead box protein O3 (AF6q21 protein) (Forkhead in rhabdomyosarcoma-like 1)

Source: Rabbit

Applications: WB; ELISA

Dilution: WB 1:500-2000, ELISA 1:10000-20000

Reactivity: Human; Mouse; Rat

Immunogen: Synthesized peptide derived from human FKHRL1 Polyclonal

Storage and Stability: -20°C/1 year

Clonality: Polyclonal

Isotype: IgG

Concentration: 1 mg/ml

Observed Band (KD): 65kD

Human Gene ID: 2309

Human SWISS Prot NO: O43524

Subcellular Location: 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).

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FKHRL1 rabbit pAb - ES8898

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