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Key Documents

07-1341

Sigma-Aldrich

Anti-PHLPP1 Antibody

from rabbit, purified by affinity chromatography

Synonym(s):

PH domain and leucine rich repeat protein phosphatase, PH domain leucine-rich repeat protein phosphatase, Pleckstrin homology domain-containing family E protein 1, SCN circadian oscillatory protein, Suprachiasmatic nucleus circadian oscillatory protein

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

Quality Level

100

conjugate

conjugate

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

liquid

purified by

affinity chromatography

species reactivity

rat, mouse, human

technique(s)

immunocytochemistry: suitable
western blot: suitable

immunogen sequence

KLH-conjugated linear peptide corresponding to the C-terminus of PHLPP1.

NCBI accession no.

NP_919431

UniProt accession no.

O60346

shipped in

wet ice

storage temp.

2-8°C

Gene Information

human ... PHLPP1(23239)

General description

PHLPP1 is the protein phosphatase responsible for dephosphorylation of the Akt (Ser473) site. Akt (Ser473) is the TORC2 (mTOR) phosphorylation activation site.

Specificity

This antibody recognizes the C-terminal region of PHLPP1.

Immunogen

Epitope: C-terminus
KLH-conjugated linear peptide corresponding to the C-terminus of PHLPP1.

Application

Anti-PHLPP1 Antibody detects level of PHLPP1 & has been published & validated for use in WB & IC.
Research Category
Signaling
Research Sub Category
PI3K, Akt, & mTOR Signaling

Quality

Evaluated by Western Blot in Human brain tissue lysate.
Western Blot Analysis: A 1:1,000 dilution of this antibody detected PHLPP1 in Human brain tissue lysate.

Target description

134 kDa Observed at 110 kDa

Physical form

Affinity purified
Purified rabbit serum in buffer containing 0.1 M Tris-glycine, pH 7.4, 150 mM NaCl and 0.05% sodium azide.

Storage and Stability

Maintain refrigerated at 2-8°C for 1 year from date of receipt.

Analysis Note

Control
Human brain tissue lysate

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Saida Abdelli et al.
PloS one, 7(5), e35997-e35997 (2012-05-09)
We have recently shown that silencing of the brain/islet specific c-Jun N-terminal Kinase3 (JNK3) isoform enhances both basal and cytokine-induced beta-cell apoptosis, whereas silencing of JNK1 or JNK2 has opposite effects. While it is known that JNK1 or JNK2 may
A molecular brake controls the magnitude of long-term potentiation.
Wang, Y; Zhu, G; Briz, V; Hsu, YT; Bi, X; Baudry, M
Nature Communications null
Julia Fischer et al.
Proceedings of the National Academy of Sciences of the United States of America, 116(33), 16551-16560 (2019-07-28)
The dynamic interplay between metabolism and immune responses in health and disease, by which different immune cells impact on metabolic processes, are being increasingly appreciated. However, the potential of master regulators of metabolism to control innate immunity are less understood.
Marcelline K Hanson et al.
PloS one, 16(6), e0251732-e0251732 (2021-06-19)
Prior studies demonstrated that deletion of the protein phosphatase Phlpp1 in Ctsk-Cre expressing cells enhances bone mass, characterized by diminished osteoclast activity and increased coupling to bone formation. Due to non-specific expression of Ctsk-Cre, the definitive mechanism for this observation
Yubin Wang et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 33(48), 18880-18892 (2013-11-29)
Prolonged calpain activation is widely recognized as a key component of neurodegeneration in a variety of pathological conditions. Numerous reports have also indicated that synaptic activation of NMDA receptors (NMDARs) provides neuroprotection against a variety of insults. Here, we report
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