PPP1R16B

Last update 08 May 2025

Basic Info

Synonyms

ANKRD4, Ankyrin repeat domain-containing protein 4, CAAX box protein TIMAP

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Introduction

Regulator of protein phosphatase 1 (PP1) that acts as a positive regulator of pulmonary endothelial cell (EC) barrier function (PubMed:18586956). Involved in the regulation of the PI3K/AKT signaling pathway, angiogenesis and endothelial cell proliferation (PubMed:25007873). Regulates angiogenesis and endothelial cell proliferation through the control of ECE1 dephosphorylation, trafficking and activity (By similarity). Protects the endothelial barrier from lipopolysaccharide (LPS)-induced vascular leakage (By similarity). Involved in the regulation of endothelial cell filopodia extension (By similarity). May be a downstream target for TGF-beta1 signaling cascade in endothelial cells (PubMed:16263087, PubMed:18586956). Involved in PKA-mediated moesin dephosphorylation which is important in EC barrier protection against thrombin stimulation (PubMed:18586956). Promotes the interaction of PPP1CA with RPSA/LAMR1 and in turn facilitates the dephosphorylation of RPSA/LAMR1 (PubMed:16263087). Involved in the dephosphorylation of EEF1A1 (PubMed:26497934).

100 Clinical Results associated with PPP1R16B

100 Translational Medicine associated with PPP1R16B

0 Patents (Medical) associated with PPP1R16B

Literatures (Medical) associated with PPP1R16B

01 Dec 2024·American Journal of Physiology-Cell Physiology

Hypoxia-induced TIMAP upregulation in endothelial cells and TIMAP-dependent tumor angiogenesis

Article

Author: Li, Laiji ; Azad, Abul K. ; Alavi, Parnian ; Hussain, Aashiq ; Aburahess, Salah ; Ballermann, Barbara J. ; Obeidat, Marya ; Jahroudi, Nadia

The protein phosphatase 1 regulatory subunit TGFβ-inhibited membrane associated protein (TIMAP), known to activate AKT in endothelial cells (EC), was shown here to be repressed by bone morphogenetic factor 9 (BMP9). Hypoxia and angiogenic growth factors induced TIMAP expression by inhibiting the BMP9 pathway. In a mouse breast cancer model, TIMAP deletion inhibited tumor angiogenesis and tumor growth. Therefore, the proangiogenic functions of TIMAP are induced by hypoxia and angiogenic growth factors.

01 Jun 2024·Medical Molecular Morphology

Clinical and molecular characteristics of Jordanian oropharyngeal cancer patients according to P16 expression: a retrospective study and a report of a novel biomarker

Article

Author: Algargaz, Wisam ; Barukba, Marwa ; Barakat, Farid ; Mohamad, Issa ; Bodoor, Khaldon ; Obeidat, Marya ; Al Bashir, Samir

The purpose of this study was to assess the clinicopathological features of oropharyngeal cancer patients in Jordan based on their HPV status. Sixty-nine biopsies from two hospitals were included. Tissue microarrays were prepared from formalin-fixed paraffin-embedded (FFPE) specimens and stained with antibodies for CDKN2A/P16, EGFR, PI3K, PTEN, AKT, pS473AKT, PS2mTOR, and TIMAP. The cohort was divided according to P16 expression. Chi-square test and survival analyses were employed to evaluate the variations among the study variables and determine the prognostic factors, respectively. P16 expression was found in 55.1% of patients; however, there was no significant association between P16 expression and the patients' clinicopathological features. The Kaplan-Meier test revealed that smoking in P16-positive group and younger age (< 58 years) negatively impacted disease-free survival (DFS) (P = 0.04 and P = 0.003, respectively). Multivariate Cox regression test indicated that smoking, age, PI3K, and AKT were negative predictors of DFS (P = 0.021, P = 0.002, P = 0.021, and P = 0.009, respectively), while TIMAP was a positive predictor (P = 0.045). Elevated P16 expression is found in more than half of the patients' specimens. DFS is negatively affected by younger age and the combined effect of smoking and P16 overexpression. TIMAP is overexpressed in P16-positive oropharyngeal cancer, and it is a favorable predictor of DFS.

01 Jan 2024·Journal of Developmental Origins of Health and Disease

Methylation profiles at birth linked to early childhood obesity

Article

Author: Paul, Ian M ; Hohman, Emily E ; Craig, Sarah J C ; Reimherr, Matthew L ; Makova, Kateryna D ; Chiaromonte, Francesca ; Savage, Jennifer S ; Lariviere, Delphine ; Wright, Robert O

AbstractChildhood obesity represents a significant global health concern and identifying its risk factors is crucial for developing intervention programs. Many “omics” factors associated with the risk of developing obesity have been identified, including genomic, microbiomic, and epigenomic factors. Here, using a sample of 48 infants, we investigated how the methylation profiles in cord blood and placenta at birth were associated with weight outcomes (specifically, conditional weight gain, body mass index, and weight-for-length ratio) at age six months. We characterized genome-wide DNA methylation profiles using the Illumina Infinium MethylationEpic chip, and incorporated information on child and maternal health, and various environmental factors into the analysis. We used regression analysis to identify genes with methylation profiles most predictive of infant weight outcomes, finding a total of 23 relevant genes in cord blood and 10 in placenta. Notably, in cord blood, the methylation profiles of three genes (PLIN4, UBE2F, and PPP1R16B) were associated with all three weight outcomes, which are also associated with weight outcomes in an independent cohort suggesting a strong relationship with weight trajectories in the first six months after birth. Additionally, we developed a Methylation Risk Score (MRS) that could be used to identify children most at risk for developing childhood obesity. While many of the genes identified by our analysis have been associated with weight-related traits (e.g., glucose metabolism, BMI, or hip-to-waist ratio) in previous genome-wide association and variant studies, our analysis implicated several others, whose involvement in the obesity phenotype should be evaluated in future functional investigations.

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PPP1R16B

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