07-1341
Anti-PHLPP1 Antibody
from rabbit, purified by affinity chromatography
동의어(들):
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
로그인조직 및 계약 가격 보기
모든 사진(3)
About This Item
UNSPSC 코드:
12352203
eCl@ss:
32160702
NACRES:
NA.41
추천 제품
생물학적 소스
rabbit
Quality Level
결합
conjugate
항체 형태
affinity isolated antibody
항체 생산 유형
primary antibodies
클론
polyclonal
형태
liquid
정제법
affinity chromatography
종 반응성
rat, mouse, human
기술
immunocytochemistry: suitable
western blot: suitable
면역원 서열
KLH-conjugated linear peptide corresponding to the C-terminus of PHLPP1.
NCBI 수납 번호
UniProt 수납 번호
배송 상태
wet ice
저장 온도
2-8°C
유전자 정보
human ... PHLPP1(23239)
일반 설명
PHLPP1 is the protein phosphatase responsible for dephosphorylation of the Akt (Ser473) site. Akt (Ser473) is the TORC2 (mTOR) phosphorylation activation site.
특이성
This antibody recognizes the C-terminal region of PHLPP1.
면역원
Epitope: C-terminus
KLH-conjugated linear peptide corresponding to the C-terminus of PHLPP1.
애플리케이션
Anti-PHLPP1 Antibody detects level of PHLPP1 & has been published & validated for use in WB & IC.
Research Category
Signaling
Signaling
Research Sub Category
PI3K, Akt, & mTOR Signaling
PI3K, Akt, & mTOR Signaling
품질
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.
Western Blot Analysis: A 1:1,000 dilution of this antibody detected PHLPP1 in Human brain tissue lysate.
표적 설명
134 kDa Observed at 110 kDa
물리적 형태
Affinity purified
Purified rabbit serum in buffer containing 0.1 M Tris-glycine, pH 7.4, 150 mM NaCl and 0.05% sodium azide.
저장 및 안정성
Maintain refrigerated at 2-8°C for 1 year from date of receipt.
분석 메모
Control
Human brain tissue lysate
Human brain tissue lysate
기타 정보
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
면책조항
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
시험 성적서(COA)
제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.
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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