QuantiSir Specific Gene Knockdown Quantification Kit For Signal Transduction _ PKA RII (96 assays)
- Known as:
- QuantiSir Specific Gene Knockdown Quantification Kit Signal Transduction _ PKA RII (96 tests)
- Catalog number:
- P-5008-PKARII-96
- Category:
- Peptides
- Supplier:
- EpigenTek
- Gene target:
- QuantiSir Specific Gene Knockdown Quantification Kit For Signal Transduction _ PKA RII (96 assays)
Related genes to: QuantiSir Specific Gene Knockdown Quantification Kit For Signal Transduction _ PKA RII (96 assays)
- Gene:
- FOXD3 NIH gene
- Name:
- forkhead box D3
- Previous symbol:
- -
- Synonyms:
- Genesis, HFH2
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-22
- Date modifiied:
- 2015-08-25
Related products to: QuantiSir Specific Gene Knockdown Quantification Kit For Signal Transduction _ PKA RII (96 assays)
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Sizeα - Calcitonin Gene Related Peptide, α - CGRP, rat(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit(1-Kit) 14,15-DHET sEH activity ELISA Kit(1-Kit) 14,15-EET DHET Hypertension ELISA Kit Related articles to: QuantiSir Specific Gene Knockdown Quantification Kit For Signal Transduction _ PKA RII (96 assays)
- Hyperglycemia in pregnancy can increase the risk of congenital disorders, but little is known about craniofacial skeleton malformation and its corresponding medication. Our study first used meta-analysis to review the previous findings. Second, baicalin, an antioxidant, was chosen to counteract high glucose-induced craniofacial skeleton malformation. Its effectiveness was then tested by exposing chicken embryos to a combination of high glucose (HG, 50 mM) and 6 μM baicalin. Third, whole-mount immunofluorescence staining and hybridization revealed that baicalin administration could reverse HG-inhibited neural crest cells (NCC) delamination and migration through upregulating the expression of Pax7 and Foxd3, and mitigate the disordered epithelial-mesenchymal transition (EMT) process by regulating corresponding adhesion molecules and transcription factors (i.e., E-cadherin, N-cadherin, Cadherin 6B, Slug and Msx1). Finally, through bioinformatic analysis and cellular thermal shift assay, we identified the AKR1B1 gene as a potential target. In summary, these findings suggest that baicalin could be used as a therapeutic agent for high glucose-induced craniofacial skeleton malformation. - Source: PubMed
Publication date: 2024/03/07
Lu Jia-QiLuo Zhi-YanSun ChengyangWang Si-MiaoSun DixiangHuang Ruo-JingYang XuesongDing YongWang Guang - To elucidate the pro-tumorigenic role of IncRNA FOXD3-AS1 in glioblastoma. - Source: PubMed
Huang ConggangShao TingDuan FaliangLi RuixueLuo MingHuang QiaochunWang YuanLuo Zhihua - To explore the role of substrate stiffness and the mechanism beneath corneal endothelial cells' (CECs') stemness maintenance and differentiation. - Source: PubMed
Liu ShutingChen HuaXie HuataoLiu XinZhang Mingchang - The mesenchymal stem cells (MSCs) with characterized by their multipotency and capacity to differentiate into various tissue cell types, have led to their incorporation in regenerative medicine research. However, the limited numbers of MSCs in the human body and their diverse differentiation capabilities in tissues highlight the need for exploring alternative regenerative cell sources. In this study, therefore, we conducted molecular level examinations to determine whether pericytes, specialized cell communities situated near blood vessels, could serve as a substitute for human bone marrow-derived mesenchymal stem cells (hBM-MSCs). In this context, the potential application of pericytes surrounds the vessels when MSCs are insufficient for functional purposes. - Source: PubMed
Publication date: 2024/03/02
Polat SelenYazir YusufhanDuruksu GökhanKiliç Kamil CanMert SerapGacar GülçinÖncel Duman BüşraHalbutoğullari Zehra Seda - Ischemic stroke is one of the most vital causes of high neurological morbidity and mortality in the world. Preconditioning exercise is considered as the primary prevention of stroke to resistance to subsequent injury. We tried to research the underlying biological mechanisms of this exercise. Forty-two SD rats were randomly divided into three groups: middle cerebral artery occlusion (MCAO) group, exercise group with MCAO (EX + MCAO) group, and sham group, with 14 rats in each group. The EX + MCAO group underwent exercise preconditioning for 3 weeks before occlusion, and the other two groups were fed and exercised normally. After 3 weeks, MCAO model was made by thread plug method in the EX + MCAO group and MCAO group. After successful modeling, the Longa scale was used to evaluate the neurological impairment of rats at day 0, day 1, and day 2. The rats in each group were killed on the third day after modeling. TTC staining measured the infarct volume of each group. The morphology and apoptosis of cortical cells were observed by HE and Tunel staining. Three rats in each group underwent high-throughput sequencing. Bioinformatic analysis was used to find the deferentially expressed genes (DEGs) and predict the transcription factor binding sites (TFBS) of the next-generation sequencing results. Gene enrichment (GSEA) was used to analyze potential functional genes and their corresponding signaling pathways. The Longa scale showed EX + MCAO group had the neurological function better than the modeling group (P < 0.001). TTC staining showed that the infarct size of EX + MCAO group was less than MCAO group (P < 0.05). HE and Tunel staining showed that the cells in the EX + MCAO group and the sham group had normal morphology and fewer apoptotic cells than MCAO group. A new gene named 7994 was discovered and TFBS of this gene was predicted, which could interact with key genes such as Foxd3, Foxa2, NR4A2, SP1, CEBPA, and SOX10. GSEA showed that EX + MCAO group could promote and regulate angiogenesis and apoptosis through PI3K-AKT pathway. Preconditioning exercise could improve nerve function and reduce infarct size in rats. The underlying mechanism is to regulate the PI3K-AKT pathway through several key genes, promote cerebral angiogenesis, and reduce apoptosis. - Source: PubMed
Publication date: 2024/02/29
Li KaiGao Zhen-KunGuo Yi-ShaShen Xin-YaHan YuYuan MeiBi Xia