Ask about this productRelated genes to: PKIG antibody
- Gene:
- PKIG NIH gene
- Name:
- cAMP-dependent protein kinase inhibitor gamma
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-07
- Date modifiied:
- 2016-12-21
Related products to: PKIG antibody
Related articles to: PKIG antibody
- Cryopreservation of human ovarian tissue is a technology for patients undergoing aggressive anticancer treatments. This technology includes the following stages: saturation by permeable cryoprotectants, freezing, thawing, removal of cryoprotectants, as well as tissues or culture. - Source: PubMed
Publication date: 2025/05/02
Wang WanxueTodorov PlamenIsachenko EvgeniaRahimi GoharMerzenich MarkusMallmann-Gottschalk NinaZhou YangYao JilongLi XuemeiIsachenko Volodimir - In recent years, several giant pandas have suffered from testicular tumor, which has seriously affected giant panda health. However, the pathogenesis of testicular tumor in giant panda is still unclear. Studies have shown that miRNAs are involved in the occurrence and development of a variety of cancers. However, the effect of miRNAs on giant panda testicular tumor has been little studied. Therefore, this study explored the pathogenesis of giant panda testicular tumor through miRNA and mRNA sequencing, and screened out diagnostic markers of testicular tumor. - Source: PubMed
Publication date: 2024/11/15
Zhu YanHuang ZhiLi CaiwuLi ChengyaoWei MingDeng LinhuaDeng WenwenZhou XiaoWu KaiYang BoQu YuanyuanLiu QinChen XuemeiLi DeshengWang Chengdong - Lung cancer is the leading cause of cancer-related death worldwide, and patients have limited survival benefits from traditional treatments such as surgery, radiotherapy and chemotherapy. As a new treatment for lung cancer, immunotherapy has significantly prolonged the overall survival (OS) of patients. However, only some patients can benefit from it. We need to explore immunotherapy biomarkers more deeply to screen for advantages. - Source: PubMed
Liu QingLi HaitianLi BinRen MeiyuLi ZhenqingChen YuzhenZheng ZhizhongMeng YuqiFeng Haiming - The aim of this investigation was to study the expression of genes encoding cAMP-activated protein kinase catalytic and regulatory A subunits (PRKACA and PRKAR1A) and related proteins such as cAMP-dependent protein kinase inhibitors A and G (PKIA and PKIG), catalytic subunit A of protein phosphatase 3 (PPP3CA), A-kinase anchoring protein 12 (AKAP12), and praja ring finger ubiquitin ligase 2 (PJA2) in U87 glioma cells in response to glucose deprivation in both control U87 glioma cells and cells with ERN1 (endoplasmic reticulum to nucleus signaling 1) knockdown, the major pathway of the endoplasmic reticulum stress signaling, for evaluation of possible significance of glucose deprivation in ERN1 dependent regulation of glioma growth. The expression level of PRKA related genes was studied in control (transfected by vector) and ERN1 knockdown U87 glioma cells under glucose deprivation by real-time quantitative polymerase chain reaction. It was shown that the expression level of and genes was down-regulated in control glioma cells treated by glucose deprivation, but gene was up-regulated. At the same time, the expression of four other genes (, , , and ) was resistant to this experimental condition. Furthermore, ERN1 knockdown of glioma cells significantly modified the effect glucose deprivation on the expression almost all studied genes. Thus, treatment of glioma cells with inhibited ERN1 enzymatic activity by glucose deprivation lead to a more significant down-regulation of the expression level of and to suppression gene expressions. Moreover, the ERN1 knockdown introduced up-regulation of and gene expressions in glioma cells treated by glucose deprivation and eliminated the sensitivity of gene to this experimental condition. Results of this investigation demonstrated that ERN1 knockdown significantly modified the sensitivity of most studied PRKA related gene expressions to glucose deprivation and that these changes are a result of complex interactions of variable endoplasmic reticulum stress related and unrelated regulatory factors and contributed to the suppression of glioma cell proliferation and their possibly chemoresistance. - Source: PubMed
Publication date: 2020/11/24
Ratushna Oksana O - Essential thrombocytosis (ET) is a chronic myeloproliferative disorder with an unregulated surplus of platelets. Complications of ET include stroke, heart attack, and formation of blood clots. Although platelet-enhancing mutations have been identified in ET cohorts, genetic networks causally implicated in thrombotic risk remain unestablished. In this study, we aim to identify novel ET-related miRNA-mRNA regulatory networks through comparisons of transcriptomes between healthy controls and ET patients. Four network discovery algorithms have been employed, including (a) Pearson correlation network, (b) sparse supervised canonical correlation analysis (sSCCA), (c) sparse partial correlation network analysis (SPACE), and, (d) (sparse) Bayesian network analysis-all through a combined data-driven and knowledge-based analysis. The result predicts a close relationship between an 8-miRNA set (miR-9, miR-490-5p, miR-490-3p, miR-182, miR-34a, miR-196b, miR-34b*, miR-181a-2*) and a 9-mRNA set (CAV2, LAPTM4B, TIMP1, PKIG, WASF1, MMP1, ERVH-4, NME4, HSD17B12). The majority of the identified variables have been linked to hematologic functions by a number of studies. Furthermore, it is observed that the selected mRNAs are highly relevant to ET disease, and provide an initial framework for dissecting both platelet-enhancing and functional consequences of dysregulated platelet production. - Source: PubMed
Publication date: 2018/02/08
Zhao LuWu SongHuang EryaGnatenko DimitriBahou Wadie FZhu Wei