Rabbit Polyclonal DELE antibody. N-terminal. Suitable for WB, IHC-P and reacts with Rat, Human samples. Cited in 1 publication. Immunogen corresponding to Synthetic Peptide within Human DELE1.
pH: 7.4
Preservative: 0.02% Sodium azide
Constituents: 99% PBS
WB | IHC-P | |
---|---|---|
Human | Expected | Tested |
Rat | Tested | Expected |
Species | Dilution info | Notes |
---|---|---|
Species Rat | Dilution info 1.00000-2.00000 µg/mL | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Human | Dilution info Use at an assay dependent concentration. | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Human | Dilution info 5 µg/mL | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Rat | Dilution info Use at an assay dependent concentration. | Notes - |
Protein kinase activator that acts as a key activator of the integrated stress response (ISR) following various stresses, such as iron deficiency, mitochondrial stress or mitochondrial DNA breaks (PubMed:32132706, PubMed:32132707, PubMed:35388015, PubMed:37327776, PubMed:37550454, PubMed:37832546, PubMed:38340717). Detects impaired protein import and processing in mitochondria, activating the ISR (PubMed:35388015). May also required for the induction of death receptor-mediated apoptosis through the regulation of caspase activation (PubMed:20563667). DAP3-binding cell death enhancer 1. Protein kinase activator that activates the ISR in response to iron deficiency: iron deficiency impairs mitochondrial import, promoting DELE1 localization at the mitochondrial surface, where it binds and activates EIF2AK1/HRI to trigger the ISR. DAP3-binding cell death enhancer 1 short form. Protein kinase activator generated by protein cleavage in response to mitochondrial stress, which accumulates in the cytosol and specifically binds to and activates the protein kinase activity of EIF2AK1/HRI (PubMed:32132706, PubMed:32132707, PubMed:37327776, PubMed:37550454, PubMed:37832546, PubMed:38340717). It thereby activates the integrated stress response (ISR): EIF2AK1/HRI activation promotes eIF-2-alpha (EIF2S1) phosphorylation, leading to a decrease in global protein synthesis and the induction of selected genes, including the transcription factor ATF4, the master transcriptional regulator of the ISR (PubMed:32132706, PubMed:32132707, PubMed:37327776, PubMed:37550454, PubMed:37832546). Also acts as an activator of PRKN-independent mitophagy: activates the protein kinase activity of EIF2AK1/HRI in response to mitochondrial damage, promoting eIF-2-alpha (EIF2S1) phosphorylation, leading to mitochondrial localization of EIF2S1 followed by induction of mitophagy (PubMed:38340717).
DELE, KIAA0141, DELE1, DAP3-binding cell death enhancer 1, Death ligand signal enhancer, DELE1(L)
Rabbit Polyclonal DELE antibody. N-terminal. Suitable for WB, IHC-P and reacts with Rat, Human samples. Cited in 1 publication. Immunogen corresponding to Synthetic Peptide within Human DELE1.
pH: 7.4
Preservative: 0.02% Sodium azide
Constituents: 99% PBS
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DELE also known as DAP3-binding cell death enhancer homolog or KIAA0141 is a protein involved in the regulation of apoptosis. DELE has a molecular mass of approximately 50 kDa. It is expressed in various tissues including the liver heart and kidneys and plays a role in modulating cell death processes. It participates in the apoptotic pathway by interacting with other proteins involved in cell death regulation enhancing apoptosis signals through its interactions.
DELE enhances caspase activation in response to apoptotic stimuli facilitating cell death processes. It functions as part of a complex that includes DAP3 and other apoptotic proteins helping to amplify apoptotic signals that lead to mitochondria-mediated apoptosis. By doing so DELE contributes to the maintenance of cellular homeostasis by eliminating damaged or unwanted cells therefore participating in normal cellular turnover and response to stress signals.
The protein is an important player in the intrinsic apoptotic pathway which is activated by mitochondrial signals. It closely interacts with proteins such as BAX and BAK which are known to promote mitochondrial dysfunction leading to cytochrome c release and caspase activation. DELE is also linked with pathways involving TNF-alpha a cytokine that can initiate apoptosis through extrinsic and intrinsic pathways reflecting its involvement in cellular responses to stress and damage.
DELE has been associated with cancer and neurodegenerative diseases. Its dysregulation can lead to either excessive or inadequate apoptosis promoting tumorigenesis or allowing for cellular accumulation and subsequent disorders. DELE's interaction with p53 a prominent tumor suppressor protein highlights its role in maintaining genomic stability and preventing cancer development. In the context of neurodegenerative diseases altered DELE expression or function may contribute to the inappropriate survival of damaged neurons or excessive neuronal death therefore influencing disease progression.
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All lanes: Western blot - Anti-DELE antibody - N-terminal (ab189958) at 1 µg/mL
Lane 1: Rat brain tissue lysate
Lane 2: Rat brain tissue lysate with Blocking peptide
Predicted band size: 56 kDa
Immunohistochemical analysis of formalin-fixed, paraffin-embedded human brain cortex labeling DELE with ab189958 at 5 μg/ml.
Immunofluorescence analysis of human brain labeling DELE with ab189958 at 20 μg/ml.
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