PDPK2P

Last update 08 May 2025

Basic Info

Synonyms

3-phosphoinositide dependent protein kinase 2, pseudogene, 3-phosphoinositide-dependent protein kinase 2 pseudogene, PDPK2

+ [2]

Introduction

Phosphorylates and activates not only PKB/AKT, but also PKA, PKC-zeta, RPS6KA1 and RPS6KB1. May play a general role in signaling processes and in development (By similarity).

100 Clinical Results associated with PDPK2P

100 Translational Medicine associated with PDPK2P

0 Patents (Medical) associated with PDPK2P

Literatures (Medical) associated with PDPK2P

01 Nov 2020·The Journal of BiochemistryQ4 · BIOLOGY

Long non-coding RNA ABHD11-AS1 boosts gastric cancer development by regulating miR-361-3p/PDPK1 signalling

Q4 · BIOLOGY

Article

Author: Cao, Jie ; Xin, Hairong ; Yan, Zhifeng

AbstractGastric cancer (GC) is one of the most common cancers in gastrointestinal malignant tumours. Long non-coding RNAs were widely reported to play a significant role in the regulation of occurrence or development of tumours. Bioinformatics analysis and a wide range of experiments were conducted to explore the expression status, specific function and molecular mechanism of long non-coding RNA ABHD11 antisense RNA 1 (ABHD11-AS1). ABHD11-AS1 knockdown repressed cell proliferation but enhanced cell apoptosis in function. We proved that miR-361-3p directly combines with the 3′wUTR of PDPK2 and ABHD11-AS1 cooperated with miR-361-3p to modulate PDPK2 mRNA and protein levels. Rescue assays confirmed that the miR-361-3p silence reversed the suppressive effect of ABHD11-AS1 deficiency. In summary, ABHD11-AS1 boosts GC development by regulating miR-361-3p/PDPK1 signalling.

01 Oct 2019·Molecular OncologyQ2 · MEDICINE

lncRNA‐PDPK2P promotes hepatocellular carcinoma progression through the PDK1/AKT/Caspase 3 pathway

Q2 · MEDICINE

ArticleOA

Author: Chen, Shuxian ; Wang, Chusi ; Brand, David ; Zhao, Jingyuan ; Zhao, Jun ; Wang, Julie ; Pan, Weidong ; Fang, Qiannan ; Xue, Youqiu ; Huang, Feng ; Huang, Zhiyi ; Li, Wen ; Zheng, Song Guo

Hepatocellular carcinoma (HCC) is a malignancy with one of the worst prognoses. Long noncoding RNA (lncRNA) are emerging as an important regulator of gene expression and function, leading to the development of cancer. The aim of this study was to determine the relationship between lncRNA and HCC and to further guide clinical therapy. lncRNA in HCC and adjacent tissues were screened, and the correlation between lncRNA‐PDPK2P expression in liver tissues and the pathological characteristics and severity of HCC was assessed. The effects of PDPK2P on HCC proliferation, apoptosis, metastasis, and invasion were also systematically investigated via CCK‐8 assay, flow cytometry, scratch wound healing, and transwell assay, respectively. The relationship between PDPK2P and PDK1 was verified by RNA pull‐down, rescue experiments and western blot. lncRNA‐PDPK2P was highly expressed in HCC tissues with a distinct positive correlation between PDPK2P and PDK1, and the upregulation was clinically associated with a larger tumor embolus, low differentiation, and poor survival. Mechanistically, lncRNA‐PDPK2P interacted with PDK1 and promoted HCC progression through the PDK1/AKT/caspase 3 signaling pathway. lncRNA‐PDPK2P can promote HCC progression, suggesting it may be a clinically valuable biomarker and serve as a molecular target for the diagnosis, prognosis, and therapy of hepatocellular carcinoma.

01 Jun 2014·Journal of the American College of CardiologyQ1 · MEDICINE

Simultaneous Adrenal and Cardiac G-Protein–Coupled Receptor-Gβγ Inhibition Halts Heart Failure Progression

Q1 · MEDICINE

Article

Author: Travers, Joshua G ; Moalem, Jacob ; Mickelsen, Deanne M ; Wegman, Katherine M ; Blaxall, Burns C ; Kamal, Fadia A ; Hammes, Stephen R ; Smrcka, Alan V

OBJECTIVESThe authors propose simultaneous inhibition of Gβγ signaling in the heart and the adrenal gland as a novel therapeutic approach for heart failure (HF).BACKGROUNDElevated sympathetic nervous system activity is a salient characteristic of HF progression. It causes pathologic desensitization of β-adrenergic receptors (β-AR), facilitated predominantly through Gβγ-mediated signaling. The adrenal glands are key contributors to the chronically elevated plasma catecholamine levels observed in HF, where adrenal α2-AR feedback inhibitory function is impaired also through Gβγ-mediated signaling.METHODSWe investigated the efficacy of a small molecule Gβγ inhibitor, gallein, in a clinically relevant, pressure-overload model of HF.RESULTSDaily gallein treatment (10 mg/kg/day), initiated 4 weeks after transverse aortic constriction, improved survival and cardiac function and attenuated cardiac remodeling. Mechanistically, gallein restored β-AR membrane density in cardiomyocytes, attenuated Gβγ-mediated G-protein-coupled receptor kinase 2-phosphoinositide 3-kinase γ membrane recruitment, and reduced Akt (protein kinase B) and glycogen synthase kinase 3β phosphorylation. Gallein also reduced circulating plasma catecholamine levels and catecholamine production in isolated mouse adrenal glands by restoring adrenal α2-AR feedback inhibition. In human adrenal endocrine tumors (pheochromocytoma), gallein attenuated catecholamine secretion, as well as G-protein-coupled receptor kinase 2 expression and membrane translocation.CONCLUSIONSThese data suggest small molecule Gβγ inhibition as a systemic pharmacologic therapy for HF by simultaneously normalizing pathologic adrenergic/Gβγ signaling in both the heart and the adrenal gland. Our data also suggest important endocrine/cardiovascular interactions and a possible role for small molecule Gβγ inhibition in treating endocrine tumors such as pheochromocytoma, in addition to HF.

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PDPK2P

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