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Search results for: AKAP12

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#34122523   2021/05/26 To Up

Development and Validation of a Hypoxia-Related Signature for Predicting Survival Outcomes in Patients With Bladder Cancer.

This study aimed to develop and validate a hypoxia signature for predicting survival outcomes in patients with bladder cancer.
Facai Zhang, Xiaoming Wang, Yunjin Bai, Huan Hu, Yubo Yang, Jiahao Wang, Yin Tang, Honggui Ma, Dechao Feng, Dengxiong Li, Ping Han

2911 related Products with: Development and Validation of a Hypoxia-Related Signature for Predicting Survival Outcomes in Patients With Bladder Cancer.



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#34093646   2021/05/21 To Up

Goat : Indel Mutation Detection, Association Analysis With Litter Size and Alternative Splicing Variant Expression.

A-kinase anchoring protein 12 () plays key roles in male germ cells and female ovarian granulosa cells, whereas its influence on livestock litter size remains unclear. Herein we detected the genetic variants of gene and their effects on litter size as well as alternative splicing variants expression in Shaanbei white cashmere (SBWC) goats, aiming at exploring theoretical basis for goat molecular breeding. We identified two Insertion/deletions (Indels) (7- and 13-bp) within the gene. Statistical analyses demonstrated that the 13-bp indel mutation in the 3' UTR was significantly associated with litter size ( = 1,019), and the carriers with DD genotypes presented lower litter sizes compared with other carriers ( < 0.01). Bioinformatics analysis predicted that this 13-bp deletion sequence could bind to the seed region of miR-181, which has been documented to suppress porcine reproductive and respiratory syndrome virus (PRRSV) infection by targeting PRRSV receptor CD163 and affect the pig litter size. Therefore, luciferase assay for this 13-bp indel binding with miRNA-181 was performed, and the luciferase activity of pcDNA-miR-181-13bp-Deletion-allele vector was significantly lower than that of the pcDNA-miR-181-13bp-Insertion-allele vector ( < 0.05), suggesting the reduced binding capability with miR-181 in DD genotype. Given that alternative spliced variants and their expression considerably account for the Indel genetic effects on phenotypic traits, we therefore detected the expression of the alternative spliced variants in different tissues and identified that exhibited the highest expression levels in testis tissues. Interestingly, the expression levels of homozygote DD carriers were significantly lower than that of individuals with heterozygote ID, in both testis and ovarian tissues ( < 0.05), which is consistent with the effect of the 13-bp deletion on the reduced litter size. Taken together, our results here suggest that this 13-bp indel mutation within goat might be utilized as a novel molecular marker for improving litter size in goat breeding.
Zihong Kang, Yangyang Bai, Xianyong Lan, Haiyu Zhao

1817 related Products with: Goat : Indel Mutation Detection, Association Analysis With Litter Size and Alternative Splicing Variant Expression.

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#34023860   2021/05/22 To Up

Upregulated PPARG2 facilitates interaction with demethylated AKAP12 gene promoter and suppresses proliferation in prostate cancer.

Prostate cancer (PCA) is one of the most common male genitourinary tumors. However, the molecular mechanisms involved in the occurrence and progression of PCA have not been fully clarified. The present study aimed to investigate the biological function and molecular mechanism of the nuclear receptor peroxisome proliferator-activated receptor gamma 2 (PPARG2) in PCA. Our results revealed that PPARG2 was downregulated in PCA, and overexpression of PPARG2 inhibited cell migration, colony formation, invasion and induced cell cycle arrest of PCA cells in vitro. In addition, PPARG2 overexpression modulated the activation of the Akt signaling pathway, as well as inhibited tumor growth in vivo. Moreover, mechanistic analysis revealed that PPARG2 overexpression induced increased expression level of miR-200b-3p, which targeted 3' UTR of the downstream targets DNMT3A/3B, and facilitated interaction with demethylated AKAP12 gene promoter and suppressed cell proliferation in PCA. Our findings provided the first evidence for a novel PPARG2-AKAP12 axis mediated epigenetic regulatory network. The study identified a molecular mechanism involving an epigenetic modification that could be possibly targeted as an antitumoral strategy against prostate cancer.
Feng Li, Tingting Lu, Dongmei Liu, Chong Zhang, Yonghui Zhang, Fulu Dong

2582 related Products with: Upregulated PPARG2 facilitates interaction with demethylated AKAP12 gene promoter and suppresses proliferation in prostate cancer.



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#33885249   2020/11/24 To Up

Glucose deprivation affects the expression of genes encoding cAMP-activated protein kinase and related proteins in U87 glioma cells in ERN1 dependent manner.

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.
Oksana O Ratushna

2644 related Products with: Glucose deprivation affects the expression of genes encoding cAMP-activated protein kinase and related proteins in U87 glioma cells in ERN1 dependent manner.

2 Pieces/Box2 Pieces/Box1 mg50 502100010501 mL50

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#33853673   2021/04/14 To Up

Novel targetable FGFR2 and FGFR3 alterations in glioblastoma associate with aggressive phenotype and distinct gene expression programs.

Prognostic molecular subgrouping of glioblastoma is an ongoing effort and the current classification includes IDH-wild-type and IDH-mutant entities, the latter showing significantly better prognosis. We performed a comparative integrated analysis of the FGFR glioblastoma subgroup consisting of 5 cases from a prospective 101-patient-cohort. FGFR alterations included FGFR2-TACC2 and FGFR2 amplifications arising in a multifocal IDH-mutant glioblastoma with unexpected 2.5-month patient survival, novel FGFR3 carboxy-terminal duplication and FGFR3-TLN1 fusion, and two previously described FGFR3-TACC3 fusions. The FGFR2 tumors showed additional mutations in SERPINE1/PAI-1 and MMP16, as part of extensive extracellular matrix remodeling programs. Whole transcriptomic analysis revealed common proliferation but distinct morphogenetic gene expression programs that correlated with tumor histology. The kinase program revealed EPHA3, LTK and ALK receptor tyrosine kinase overexpression in individual FGFR tumors. Paradoxically, all FGFR-fused glioblastomas shared strong PI3K and MAPK pathway suppression effected by SPRY, DUSP and AKAP12 inhibitors, whereas the FGFR2-TACC2 tumor elicited also EGFR suppression by ERRFI1 upregulation. This integrated analysis outlined the proliferation and morphogenetic expression programs in FGFR glioblastoma, and identified four novel, clinically targetable FGFR2 and FGFR3 alterations that confer aggressive phenotype and trigger canonical pathway feedback inhibition, with important therapeutic implications.
Maria-Magdalena Georgescu, Mohammad Zahidul Islam, Yan Li, James Traylor, Anil Nanda

1281 related Products with: Novel targetable FGFR2 and FGFR3 alterations in glioblastoma associate with aggressive phenotype and distinct gene expression programs.

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#33514440   2021/01/29 To Up

Identification and validation of methylated differentially expressed miRNAs and immune infiltrate profile in EBV-associated gastric cancer.

The recent discovery of cancer/tissue specificity of miRNA has indicated its great potential as a therapeutic target. In Epstein-Barr virus-associated gastric cancer (EBVaGC), host genes are affected by extensive DNA methylation, including miRNAs. However, the role of methylated miRNA in the development of EBVaGC and immune cell infiltration has largely remained elusive.
Mansheng Zhu, Qixiang Liang, Tao Chen, Qian Kong, Gengtai Ye, Shitong Yu, Xunjun Li, Qinglie He, Hao Liu, Yanfeng Hu, Jiang Yu, Guoxin Li

2993 related Products with: Identification and validation of methylated differentially expressed miRNAs and immune infiltrate profile in EBV-associated gastric cancer.

10 mg

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#33492625   2021/01/25 To Up

Roles of A-kinase Anchor Protein 12 in Astrocyte and Oligodendrocyte Precursor Cell in Postnatal Corpus Callosum.

The formation of the corpus callosum in the postnatal period is crucial for normal neurological function, and clinical genetic studies have identified an association of 6q24-25 microdeletion in this process. However, the mechanisms underlying corpus callosum formation and its critical gene(s) are not fully understood or identified. In this study, we examined the roles of AKAP12 in postnatal corpus callosum formation by focusing on the development of glial cells, because AKAP12 is coded on 6q25.1 and has recently been shown to play roles in the regulations of glial function. In mice, the levels of AKAP12 expression was confirmed to be larger in the corpus callosum compared to the cortex, and AKAP12 levels decreased with age both in the corpus callosum and cortex regions. In addition, astrocytes expressed AKAP12 in the corpus callosum after birth, but oligodendrocyte precursor cells (OPCs), another major type of glial cell in the developing corpus callosum, did not. Furthermore, compared to wild types, Akap12 knockout mice showed smaller numbers of both astrocytes and OPCs, along with slower development of corpus callosum after birth. These findings suggest that AKAP12 signaling may be required for postnatal glial formation in the corpus callosum through cell- and non-cell autonomous mechanisms.
Hajime Takase, Gen Hamanaka, Ryo Ohtomo, Ji Hyun Park, Kelly K Chung, Irwin H Gelman, Kyu-Won Kim, Josephine Lok, Eng H Lo, Ken Arai

1817 related Products with: Roles of A-kinase Anchor Protein 12 in Astrocyte and Oligodendrocyte Precursor Cell in Postnatal Corpus Callosum.

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#33324446   2020/11/26 To Up

Multi-Omics Analysis Reveals Novel Subtypes and Driver Genes in Glioblastoma.

Glioblastoma is the most lethal malignant primary brain tumor; nevertheless, there remains a lack of accurate prognostic markers and drug targets. In this study, we analyzed 117 primary glioblastoma patients' data that contained SNP, DNA copy, DNA methylation, mRNA expression, and clinical information. After the quality of control examination, we conducted the single nucleotide polymorphism (SNP) analysis, copy number variation (CNV) analysis, and infiltrated immune cells estimate. And moreover, by using the cluster of cluster analysis (CoCA) methods, we finally divided these GBM patients into two novel subtypes, HX-1 (Cluster 1) and HX-2 (Cluster 2), which could be co-characterized by 3 methylation variable positions [cg16957313(DUSP1), cg17783509(PHOX2B), cg23432345(HOXA7)] and 15 (PCDH1, CYP27B1, LPIN3, GPR32, BCL6, OR4Q3, MAGI3, SKIV2L, PCSK5, AKAP12, UBE3B, MAP4, TP53BP1, F5, RHOBTB1) gene mutations pattern. Compared to HX-1 subtype, the HX-2 subtype was identified with higher gene co-occurring events, tumor mutation burden (TBM), and poor median overall survival [231.5 days (HX-2) vs. 445 days (HX-1), -value = 0.00053]. We believe that HX-1 and HX-2 subtypes may make sense as the potential prognostic biomarkers for patients with glioblastoma.
Yang Yuan, Pan Qi, Wang Xiang, Liu Yanhui, Li Yu, Mao Qing

2187 related Products with: Multi-Omics Analysis Reveals Novel Subtypes and Driver Genes in Glioblastoma.

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#33260683   2020/11/28 To Up

AKAP12 Supports Blood-Brain Barrier Integrity against Ischemic Stroke.

A-kinase anchor protein 12 (AKAP12) is a scaffolding protein that associates with intracellular molecules to regulate multiple signal transductions. Although the roles of AKAP12 in the central nervous system are still relatively understudied, it was previously shown that AKAP12 regulates blood-retinal barrier formation. In this study, we asked whether AKAP12 also supports the function and integrity of the blood-brain barrier (BBB). In a mouse model of focal ischemia, the expression level of AKAP12 in cerebral endothelial cells was upregulated during the acute phase of stroke. Also, in cultured cerebral endothelial cells, oxygen-glucose deprivation induced the upregulation of AKAP12. When AKAP12 expression was suppressed by an siRNA approach in cultured endothelial cells, endothelial permeability was increased along with the dysregulation of ZO-1/Claudin 5 expression. In addition, the loss of AKAP12 expression caused an upregulation/activation of the Rho kinase pathway, and treatment of Rho kinase inhibitor Y-27632 mitigated the increase of endothelial permeability in AKAP12-deficient endothelial cell cultures. These in vitro findings were confirmed by our in vivo experiments using knockout mice. Compared to wild-type mice, knockout mice showed a larger extent of BBB damage after stroke. However, the inhibition of rho kinase by Y-27632 tightened the BBB in knockout mice. These data may suggest that endogenous AKAP12 works to alleviate the damage and dysfunction of the BBB caused by ischemic stress. Therefore, the AKAP12-rho-kinase signaling pathway represents a novel therapeutic target for stroke.
Ji Hae Seo, Takakuni Maki, Nobukazu Miyamoto, Yoon Kyong Choi, Kelly K Chung, Gen Hamanaka, Ji Hyun Park, Emiri T Mandeville, Hajime Takase, Kazuhide Hayakawa, Josephine Lok, Irwin H Gelman, Kyu-Won Kim, Eng H Lo, Ken Arai

1546 related Products with: AKAP12 Supports Blood-Brain Barrier Integrity against Ischemic Stroke.

500ml130ml4800 (in case - Racked - 2ug

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