Ask about this productRelated genes to: Pkib Blocking Peptide
- Gene:
- PKIB NIH gene
- Name:
- cAMP-dependent protein kinase inhibitor beta
- Previous symbol:
- PRKACN2
- Synonyms:
- -
- Chromosome:
- 6q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-27
- Date modifiied:
- 2016-12-21
Related products to: Pkib Blocking Peptide
Related articles to: Pkib Blocking Peptide
- Cyclic AMP-dependent protein kinase A (PKA) is recognized for its pivotal involvement in various cancer types, with Protein Kinase Inhibitor Beta (PKIB) serving as an endogenous inhibitor that curtails PKA activity. Despite the documented escalation of PKIB expression in several malignancies, a comprehensive understanding of its precise mechanistic implications in human cancers remains elusive. This investigation is centered on bladder cancer (BLCA), unveiling an augmented expression of PKIB concomitant with heightened BLCA cell proliferation, migration, and invasion in vitro and augmented tumorigenic potential in an in vivo model. Mechanistically, PKIB disrupts PKA kinase activity, thereby resulting in diminished phosphorylation of the substrate target protein HSP27 at serine 15, 78, and 82. Additionally, the transcription factor MYCN exhibits an affinity for the PKIB promoter, leading to its enhanced expression in the context of BLCA. These findings reveal the oncogenic proclivity of PKIB and introduce a novel signalling pathway in BLCA, providing valuable insights into potential therapeutic targets for precise intervention. - Source: PubMed
Publication date: 2025/07/01
Liu XiaolongYin XiaoyuYuan FengLi ShiqingXiao FeiZhou FengPan XudongHo YatfaatDong ShuoXu DuanMa YunqingCao ZhengdingLei ZheSun Yi - 2,3,7,8 -tetrachlorodibenzo-p-dioxin (TCDD) is a teratogen that can induce cleft palate formation, a common birth defect. Competing endogenous RNAs (ceRNAs), including circular RNAs (circRNAs) and long non-coding RNAs (lncRNAs), indirectly regulate gene expression via sharing microRNAs (miRNAs). Nevertheless, the mechanism by which they act as ceRNAs to regulate palatal development remains to be explored in greater detail. Here, the cleft palate model of C57BL/6 N pregnant mice was constructed by gavage of TCDD (64 ug/kg) on gestation day (GD) 10.5, and the palatal shelves were taken on gestation day (GD) 14.5 for whole-transcriptome sequencing to investigate the underlying mechanisms of the roles of circRNAs and lncRNAs as ceRNAs in cleft palate. Sequencing results revealed that 293 lncRNA, 589 circRNA, 47 miRNA, and 138 messenger RNA (mRNA) were significantly dysregulated, and the cytochrome P450 (CYP) enzymes and the aryl hydrocarbon receptor (AhR) pathway play key roles in the induction of cleft palate upon exposure to TCDD. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed the function of TCDD function was mainly related to the metabolic processes of intracellular compounds, including the metabolic processes of cellular aromatic compounds and the metabolism of exogenous drugs by cytochrome P450, etc. Furthermore, quantitative reverse transcription polymerase chain reaction (qRT-PCR) indicated that the circRNA_1781/miR-30c-1-3p/PKIB and XR_380026.2/miR-1249-3p/DNAH10 ceRNA networks were hypothesized to be a hub involved in palatal development suggesting that the circRNA_1781/miR-30c-1-3p/PKIB and XR_380026.2/miR-1249-3p/DNAH10 ceRNA networks may be critical for palatogenesis, setting the foundation for the investigation of cleft palate. - Source: PubMed
Publication date: 2024/09/11
Yu ZengliZhang YaxinWang GuoxuSong ShuaixingSu HexinDuan WenjingWu YangZhang YuweiLiu Xiaozhuan - The serine-threonine kinase protein kinase A (PKA) is a cyclic AMP (cAMP)-dependent intracellular protein with multiple roles in cellular biology including metabolic and transcription regulation functions. The cAMP-dependent protein kinase inhibitor β (PKIB) is one of three known endogenous protein kinase inhibitors of PKA. The role of PKIB is not yet fully understood. Hormonal signaling is correlated with increased PKIB expression through genetic regulation, and increasing PKIB expression is associated with decreased cancer patient prognosis. Additionally, PKIB impacts cancer cell behavior through two mechanisms; the first is the nuclear modulation of transcriptional activation and the second is the regulation of oncogenic AKT signaling. The limited research into PKIB indicates the oncogenic potential of PKIB in various cancers. However, some studies suggest a role of PKIB in non-cancerous disease states. This review aims to summarize the current literature and background of PKIB regarding cancer and related issues. In particular, we will focus on cancer development and therapeutic possibilities, which are of paramount interest in PKIB oncology research. - Source: PubMed
Publication date: 2024/04/25
Musket AnnaMoorman Jonathan PZhang JinyuJiang Yong - Adenomyosis is a poorly understood gynecological disorder lacking effective treatments. Controversy persists regarding "invagination" and "metaplasia" theories. The endometrial-myometrial junction (EMJ) connects the endometrium and myometrium and is important for diagnosing and classifying adenomyosis, but its in-depth study is just beginning. Using single-cell RNA sequencing and spatial profiling, we mapped transcriptional alterations across eutopic endometrium, lesions, and EMJ. Within lesions, we identified unique epithelial (LGR5+) and invasive stromal (PKIB+) subpopulations, along with WFDC1+ progenitor cells, supporting a complex interplay between "invagination" and "metaplasia" theories of pathogenesis. Further, we observed endothelial cell heterogeneity and abnormal angiogenic signaling involving vascular endothelial growth factor and angiopoietin pathways. Cell-cell communication differed markedly between ectopic and eutopic endometrium, with aberrant signaling in lesions involving pleiotrophin, TWEAK, and WNT cascades. This study reveals unique stem cell-like and invasive cell subpopulations within adenomyosis lesions identified, dysfunctional signaling, and EMJ abnormalities critical to developing precise diagnostic and therapeutic strategies. - Source: PubMed
Chen TaoXu YiliangXu XiaocuiWang JianzhangQiu ZhiruoYu YayuanJiang XiaohongShao WanqiBai DandanWang MingzhuMei ShuyanCheng TaoWu LiGao ShaorongChe Xuan - In castration-resistant prostate cancer (CRPC), increased glucocorticoid receptor (GR) expression and ensuing transcriptional activity have been proposed as an oncogenic "bypass" mechanism in response to androgen receptor (AR) signaling inhibition (ARSi). Here, we report that GR transcriptional activity acquired following ARSi is associated with the upregulation of cyclic adenosine monophosphate (cAMP)-associated gene expression pathways in both model systems and metastatic prostate cancer patient samples. In the context of ARSi, the expression of GR-mediated genes encoding cAMP signaling pathway-associated proteins can be inhibited by treatment with selective GR modulators (SGRMs). For example, in the context of ARSi, we found that GR activation resulted in upregulation of protein kinase inhibitor beta (PKIB) mRNA and protein levels, leading to nuclear accumulation of the cAMP-dependent protein kinase A catalytic subunit (PKA-c). Increased PKA-c, in turn, is associated with increased cAMP response element-binding protein phosphorylation and activity. Furthermore, enzalutamide and SGRM combination therapy in mice bearing CRPC xenografts delayed CRPC progression compared with enzalutamide therapy alone, and reduced tumor PKIB mRNA expression. Supporting the clinical importance of GR/PKA signaling activation in CRPC, we found a significant enrichment of both cAMP pathway signaling-associated gene expression and high NR3C1 (GR) activity in patient-derived xenograft models and metastatic human CRPC samples. These findings suggest a novel mechanism linking CRPC-induced GR transcriptional activity with increased cAMP signaling in AR-antagonized CRPC. Furthermore, our findings suggest that GR-specific modulation in addition to AR antagonism may delay GR+ CRPC time to recurrence, at least in part, by inhibiting tumor cAMP/PKA pathways. - Source: PubMed
Bennett LyndaJaiswal Praveen KumarHarkless Ryan VLong Tiha MGao NingVandenburg BriannaSelman PhillipDurdana IshratLastra Ricardo RVander Griend DonaldAdelaiye-Ogala RemiSzmulewitz Russell ZConzen Suzanne D