PDE4DIP

Last update 08 May 2025

Basic Info

Synonyms

Cardiomyopathy-associated protein 2, CMYA2, KIAA0454

+ [6]

Introduction

Functions as an anchor sequestering components of the cAMP-dependent pathway to Golgi and/or centrosomes (By similarity). Participates in microtubule dynamics, promoting microtubule assembly. Depending upon the cell context, may act at the level of the Golgi apparatus or that of the centrosome (PubMed:25217626, PubMed:27666745, PubMed:28814570, PubMed:29162697). In complex with AKAP9, recruits CAMSAP2 to the Golgi apparatus and tethers non-centrosomal minus-end microtubules to the Golgi, an important step for polarized cell movement (PubMed:27666745, PubMed:28814570). In complex with AKAP9, EB1/MAPRE1 and CDK5RAP2, contributes to microtubules nucleation and extension from the centrosome to the cell periphery, a crucial process for directed cell migration, mitotic spindle orientation and cell-cycle progression (PubMed:29162697).

100 Clinical Results associated with PDE4DIP

100 Translational Medicine associated with PDE4DIP

0 Patents (Medical) associated with PDE4DIP

104

Literatures (Medical) associated with PDE4DIP

01 Feb 2025·Journal of Gastroenterology and Hepatology

Identification of Genetic Factors Related With Nonhereditary Colorectal Polyposis and Its Recurrence Through Genome‐Wide Association Study

Article

Author: Jeon, Chan Il ; Cheon, Jae Hee ; Park, Soo Jung ; Kim, Tae Il ; Jang, Jihun ; Jee, Sun Ha ; Lee, Su Hyun ; Ji, Jung Hyun ; Park, Jihye ; Park, Jae Jun

ABSTRACTBackgroundMany patients with colorectal polyposis demonstrate negative results in germline mutation test. This study aimed to uncover genetic variants associated with nonhereditary colorectal polyposis using a genome‐wide association study (GWAS).MethodsAt a single referral university hospital, between January 2012 and September 2021, 638 patients with ≥ 10 biopsy‐proven cumulative polyps on colonoscopy without germline mutations related to hereditary colorectal cancer or polyposis were included. The control group comprised 1863 individuals from the Korea Medical Institute, each having undergone at least two colonoscopies, all of which were normal. This study utilized GWAS to identify susceptibility loci for nonhereditary colorectal polyposis. Genetic differences between patients with and without ≥ 10 polyp recurrences were analyzed using Cox proportional hazards models.ResultsGWAS revealed 71 novel risk single‐nucleotide polymorphisms (SNPs) not seen in previous colorectal cancer and polyp GWAS. Five genes (UPF3A, BICRA, CBWD6, PDE4DIP, and ABCC4) overlapping seven SNPs (rs566295755, rs2770288, rs1012003, rs201270202, rs71264659, rs1699813, and rs149368557), previously linked to colorectal cancer, were identified as significant risk factors for nonhereditary colorectal polyposis. Two novel genes (CNTN4 and CNTNAP3B), not previously associated with colorectal diseases, were identified. Three SNPs (rs149368557, rs12438834, and rs9707935) were significantly associated with higher risk of recurrence of polyposis. The gene overlapping with rs149368557 was ABCC4, which was also significantly associated with an increased risk of nonhereditary colorectal polyposis.ConclusionThis study identified 71 novel risk variants for nonhereditary colorectal polyposis, with three SNPs (rs149368557, rs12438834, and rs9707935) indicating significant associations with increased risk of polyposis recurrence.

01 Dec 2024·Annals of Hematology

Construction of AML prognostic model with CYP2E1 and GALNT12 biomarkers based on golgi- associated genes

Article

Author: Wang, Ying ; Lu, Bo ; Xu, Xiao-Jun ; Lin, Chao ; Tang, Jing ; Bin, Ting

Acute myeloid leukaemia (AML) was originally an aggressive malignancy of the bone marrow and one of the deadliest forms of acute leukaemia. The 5-year mortality benefit for patients with AML was only 28.3%. Moreover, a large proportion of patients experienced frequent relapses even after remission, thus predicting a bleak prognosis. This research employed differential expression analysis of AML and normal samples sourced from the GSE30029 database, as well as weighted gene co-expression network analysis (WGCNA). We discovered differential golgi apparatus-related genes (DGARGs) specifically associated with AML. Via regressivity analysis and machine learning algorithm, the cancer genome atlas-acute myeloid leukemia (TCGA-AML) cohort developed a prognostic model using characteristic prognostic genes. The performance value of risk score was analysed using Kaplan-Meier (KM) curves and Cox regression. A predictive nomogram was developed to assess the outcome. The association between prognostic trait genes and the immune microenvironment was examined. Finally, immunoactivity and drug susceptibilities were evaluated in various risk groups identified by prognostic signature genes. A total of 77 DGARGs were obtained by differential expression analysis with WGCNA analysis. Following univariate Cox regression and LASSO regression, six prognostic signature genes (ARL5B, GALNT12, MANSC1, PDE4DIP, NCALD and CYP2E1) were utilized to develop a prognostic model. This model was calibrated via KM survival and receiver operating characteristic (ROC) curves, which concluded that it had a predictive impact on the prognosis of AML. Further analysis of the tumour microenvironment in AML patients demonstrated notable variances in immune cell APC_co_inhibition, CCR, Parainflammation, Type_I_IFN_Response, and Type_II_IFN_Response between the high-risk and low-risk groups. A prognostic model was devised in this study using six prognostic genes linked to the Golgi apparatus. The exactness of the model in guiding the prognosis of AML was established. As a result of expression validation, CYP2E1 and GALNT12 will be used as biomarkers to offer fresh insights into the prognosis and treatment of AML patients.

01 May 2024·European Journal of Haematology

Transcriptome analysis of primary adult B‐cell lineage acute lymphoblastic leukemia identifies pathogenic variants and gene fusions, and predicts subtypes for in depth molecular diagnosis

Article

Author: Schjerven, Hilde ; Munthe, Ludvig A ; Drivet, Elsa ; Podgorica, Mirjam ; Vestbøstad, Johanne ; Szodoray, Peter ; Richman, Alyssa ; Viken, Jonas Krag ; Kvam, Ann Kristin ; Frietze, Seth ; Wik, Hilde Skuterud ; Tjønnfjord, Geir E

AbstractBackgroundB‐cell acute lymphoblastic leukemia (B‐ALL) is classified into subgroups based on known driver oncogenes and molecular lesions, including translocations and recurrent mutations. However, the current diagnostic tests do not identify subtypes or oncogenic lesions for all B‐ALL samples, creating a heterogeneous B‐ALL group of unknown subtypes.MethodsWe sorted primary adult B‐ALL cells and performed transcriptome analysis by bulk RNA sequencing (RNA‐seq).ResultsTranscriptomic analysis of an adult B‐ALL cohort allowed the classification of four patient samples with subtypes that were not previously revealed by standard gene panels. The leukemia of two patients were of the DUX4 subtype and two were CRLF2+ Ph‐like B‐ALL. Furthermore, single nucleotide variant analysis detected the oncogenic NRAS‐G12D, KRAS‐G12D, and KRAS‐G13D mutations in three of the patient samples, presenting targetable mutations. Additional oncogenic variants and gene fusions were uncovered, as well as multiple variants in the PDE4DIP gene across five of the patient samples.ConclusionWe demonstrate that RNA‐seq is an effective tool for precision medicine in B‐ALL by providing comprehensive molecular profiling of leukemia cells, identifying subtype and oncogenic lesions, and stratifying patients for appropriate therapy.

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