Phosphatidylinositol 4-Phosphate 5-Kinase Type-1 Alpha (PIP5K1A) Antibody

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Description
Phosphatidylinositol 4-Phosphate 5-Kinase Type-1 Alpha (PIP5K1A) Antibody is a Rabbit polyclonal antibody for the detection of Human Phosphatidylinositol 4-Phosphate 5-Kinase Type-1 Alpha (PIP5K1A).
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Product specifications
Category | Primary Antibodies |
Immunogen Target | Phosphatidylinositol 4-Phosphate 5-Kinase Type-1 Alpha (PIP5K1A) |
Host | Rabbit |
Reactivity | Human |
Recommended Dilution | Optimal dilutions/concentrations should be determined by the end user. |
Clonality | Polyclonal |
Conjugation | Unconjugated |
Isotype | IgG |
Size 1 | 50 µg |
Size 2 | 100 µg |
Form | Liquid |
Tested Applications | ELISA, WB, IHC |
Buffer | 0.01 M PBS, pH 7.4, 50% glycerol, 0.05% Proclin-300. |
Availability | Shipped within 5-12 working days. |
Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
Dry Ice | No |
UniProt ID | Q99755 |
Gene ID | 8394 |
NCBI Accession | NP_001129108.1 |
Background | Antibody anti-PIP5K1A |
Status | RUO |
Descripción
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Phosphatidylinositol-4-Phosphate 5-Kinase Type 1 Alpha (PIP5K1A) Antibody
PIP5K1A Antibody is a Rabbit Polyclonal Antibody against PIP5K1A.
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Phosphatidylinositol-4-Phosphate 5-Kinase Type 1 Alpha (PIP5K1A) Antibody
Overexpression of phosphatidylinositol phosphate 5-kinase alpha (PIP5KIalpha), which synthesizes PIP2, suppresses apoptosis, whereas a kinase-deficient mutant does not. Protection by the wild-type PIP5KIalpha isaccompanied by decreases in the generation of activated caspases and of caspase 3-cleaved PARP. Protection is not mediated through PIP3 or Akt activation. An anti-apoptotic role for PIP (2) is substantiated by the finding that PIP5KIalpha is cleaved by caspase 3 during apoptosis, and cleavage inactivates PIP5KIalpha in vitro. Mutation of the P (4) position (D279A) of the PIP5KIalpha caspase 3 cleavage consensus prevents cleavage in vitro, and during apoptosis in vivo. Significantly, the caspase 3-resistant PIP5KIalpha mutant is more effective in suppressing apoptosis than the wild-type kinase. PIP2 is a direct regulator of apical and effector caspases in the death receptor and mitochondrial pathways, and PIP5KIalpha inactivation contributes to the progression of apoptosis.
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