PIP5K1A antibody

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935106861
info@markelab.com
name
PIP5K1A antibody
category
Primary Antibodies
provider
FineTest
reference
FNab06463
tested applications
ELISA, WB, IHC, IF

Documents del producto

Instrucciones
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Data sheet
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Product specifications

Category
Primary Antibodies
Immunogen Target
phosphatidylinositol-4-phosphate 5-kinase, type I, alpha (PIP5K1A)
Host
Rabbit
Reactivity
Human, Rat
Recommended Dilution
WB: 1:500 - 1:2000; IHC: 1:50 - 1:200; IF: 1:50 - 1:200
Clonality
polyclonal
Conjugation
Unconjugated
Isotype
IgG
Observed MW
63 kDa
Purity
≥95% as determined by SDS-PAGE
Purification
Immunogen affinity purified
Size 1
100µg
Form
liquid
Tested Applications
ELISA, WB, IHC, IF
Storage
PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months (Avoid repeated freeze / thaw cycles.)
UniProt ID
Q99755
Gene ID
8394
Alias
Phosphatidylinositol 4-phosphate 5-kinase type-1 alpha (PIP5K1-alpha, PtdIns(4)P-5-kinase 1 alpha),68 kDa type I phosphatidylinositol 4-phosphate 5-kinase alpha,Phosphatidylinositol 4-phosphate 5-kinase type I alpha (PIP5KIalpha),PIP5K1A
Background
Antibody anti-PIP5K1A
Status
RUO
Note
Mol. Weight 63 kDa

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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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