CD49_VLA{very late antigens}rabbit.pAb
- Known as:
- CD49_VLA{very late antigens}host: rabbit.pAb
- Catalog number:
- 201-20-7230
- Product Quantity:
- 0.1ml
- Category:
- -
- Supplier:
- Shanghai Sunred
- Gene target:
- CD49_VLA{very late antigens}rabbit.pAb
Related genes to: CD49_VLA{very late antigens}rabbit.pAb
- Gene:
- MAPK4 NIH gene
- Name:
- mitogen-activated protein kinase 4
- Previous symbol:
- PRKM4
- Synonyms:
- Erk3-related, Erk4
- Chromosome:
- 18q21.1-q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-08
- Date modifiied:
- 2018-02-13
Related products to: CD49_VLA{very late antigens}rabbit.pAb
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host Rabbit, Extraction-free, CE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host RabbitExtraction-freeCE-marked(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host: Rabbit, Extraction-free, CE-marked Related articles to: CD49_VLA{very late antigens}rabbit.pAb
- Peanut (Arachis hypogaea L.) is one of the most important oilseed and food crops, and the drought stress remains the primary adverse environmental factor limiting its growth and productivity. Mitogen-activated protein kinase (MAPK) cascades play crucial roles in various signal transduction pathways, affecting a wide range of physiological processes and drought stress responses in plants; however, the systematic analysis of the MAPK gene family in peanuts remains unexplored. In this study, we identified 30, 16, and 15 MAPK genes in A. hypogaea, Arachis duranensis, and Arachis ipaensis, respectively. RNA-sequencing analysis in drought-tolerant and drought-susceptible genotypes revealed that Ah_At_MAPK4 and Ah_Bt_MAPK4 were significantly upregulated under drought stress conditions, with substantially higher induction in drought-tolerant genotypes compared to drought-susceptible ones. Weighted gene co-expression network analysis further identified a drought-responsive turquoise module highly correlated with drought tolerance traits, and both Ah_At_MAPK4 and Ah_Bt_MAPK4 were identified as core regulatory components within this module. Hub gene analysis revealed these MAPKs co-express with calmodulin-binding proteins, implicating calcium signaling in drought adaptation. Three-dimensional structural modeling confirmed both proteins possess canonical bilobed kinase architecture with properly positioned Thr-Glu-Tyr motifs and intact catalytic machinery. This genome-to-structure analysis identifies Ah_At_MAPK4 and Ah_Bt_MAPK4 as key components in drought-responsive networks and provides molecular targets for enhancing drought resilience in peanut breeding. - Source: PubMed
Zhang JieMeng QingyingSanz-Saez AlvaroChen Charles - This study explored the anticancer potential of p-cymene against hepatocellular carcinoma (HCC) through computational and in vitro approaches. Bioinformatics analysis identified 635 potential targets of p-cymene, with 216 overlapping HCC-related proteins. Target interaction networks were constructed using STRING and Cytoscape, revealing key proteins involved in apoptosis, angiogenesis, and tumor progression. Molecular docking was performed using the molecular operating environment software, demonstrating strong binding affinities of p-cymene with key overlapping HCC targets, including hypoxia-inducible factor 1-alpha (HIF1A), B-cell lymphoma 2 (BCL2), cyclin-dependent kinase 9 (CDK9), Janus kinase 2 (JAK2), vascular endothelial growth factor (VEGF), mitogen-activated protein kinase 4 (MAPK4), tumor protein p53 (P53), signal transducer and activator of transcription 3 (STAT3), and caspase-3 (CASP3). HepG2 cells were treated with increasing concentrations of p-cymene (5-50 mM), and cytotoxicity was assessed using MTT, crystal violet, and trypan blue exclusion assays. Antioxidant activity was measured by evaluating superoxide dismutase (SOD) and glutathione (GSH) levels. Apoptotic markers, including CASP3, P53, VEGF, and BCL2, were quantified using ELISA. Results showed a dose-dependent reduction in HepG2 cell viability, with significant cytotoxic effects at higher p-cymene concentrations (30 and 50 mM). p-Cymene reduced oxidative stress, evident from increased SOD and GSH levels, and triggered apoptosis, as indicated by increased CASP3 and P53 expression. Additionally, BCL2 and VEGF were downregulated, suggesting inhibition of cell survival and angiogenesis. These findings highlight p-cymene's multi-targeted anticancer effects in HCC cells, supporting its further evaluation in in vivo models and potential combination therapies for improved therapeutic outcomes. - Source: PubMed
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Anwar NadiaMalik Muhammad Nasir HayatAtif MuhammadAlanzi Abdullah RAlharbi Hattan AYounis WaqasAbbas MunawarSolre Gideon F B - Hepatocellular carcinoma (HCC) is highly resistant to conventional therapies, highlighting the need for novel immunotherapeutic approaches. In the tumor microenvironment (TME), the role of proinflammatory M1 macrophages remains ambiguous. The proteins and cyclin E2 (CE2, Ccne2) are crucial for regulating hepatocyte proliferation and may be important factors driving the development of HCC. This study aimed to investigate the effects of M1 macrophages on and expression, as well as hepatocyte proliferation, in a rat model of partial hepatectomy (PH) with or without diethylnitrosamine (DEN)-induced HCC. (2) Methods: Twenty female Wistar rats were assigned to nonneoplastic (PH) or neoplastic (PH/DEN) groups. Gene expression (, ) was quantified via real-time PCR. (3) Results: Overexpression of and increased proliferation were observed in PH/DEN hepatocytes, whereas exposure to proinflammatory M1 macrophages significantly reduced their proliferative activity. expression patterns were modulated by the TME and significantly differ depending on macrophage activation status in both PH and PH/DEN-derived hepatocytes. (4) Conclusions: Our findings indicate that expression is upregulated in PH/DEN cells, with a notable decrease in the presence of M1 macrophages. In contrast, compared with control macrophages, M1 macrophages did not significantly affect expression. - Source: PubMed
Publication date: 2025/09/08
Wójcik MartaPozzo LuisaVornoli AndreaLongo VincenzoŚmiech AnnaCzerwik-Marcinkowska JoannaRozempolska-Rucińska IwonaChrapko AgnieszkaZmorzynski Szymon - Polystyrene (PS) particles, which have been recognized as emerging environmental pollutants, have increasingly been associated with various human diseases. However, their specific role and underlying mechanisms in prostate cancer development have not been fully elucidated. - Source: PubMed
Publication date: 2025/08/11
Lu ShengmingWu RuipengLi WeijianFu ZhenyuDing XuefeiLuan YangTianbao HuangHuang Yuhua - Chronic low back pain associated with intervertebral disc degeneration (IVDD) is significantly aggravated in patients with diabetes mellitus (DM); however, the underlying molecular mechanisms remain unclear. This study explored the role of the long non-coding RNA AGEAT (AGE-associated transcript) in the pathogenesis of DM-associated IVDD. Whole-transcriptome sequencing of rat nucleus pulposus cells (NPCs) treated with advanced glycation end products (AGEs) revealed a time-dependent upregulation of AGEAT. AGEAT overexpression induced NPC apoptosis, mitochondrial dysfunction, and extracellular matrix (ECM) degradation. Mechanistically, RNA fluorescence in situ hybridization localized AGEAT to the cytoplasm, where it acted as a competing endogenous RNA (ceRNA) by directly binding miR-204-5p, thereby relieving repression of its target Mapk4. Silencing AGEAT via siRNA significantly reduced apoptosis, restored mitochondrial function, and preserved ECM integrity. In vivo, intra-discal injection of AAV-sh-AGEAT in diabetic IVDD rats significantly improved disc integrity, as evidenced by a reduction in MRI Pfirrmann grade and histological preservation of NPC density and collagen II content. Collectively, these findings establish AGEAT as a key ceRNA that exacerbates diabetic IVDD via the miR-204-5p/Mapk4 axis, promoting NPC apoptosis, mitochondrial dysfunction, and ECM degradation. Targeting this pathway-through AGEAT silencing or miR-204-5p activation-represents a promising therapeutic strategy for mitigating diabetes-associated disc degeneration. This study reveals the critical role of the AGEAT/miR-204-5p/Mapk4 axis in the progression of DM-associated IVDD, suggesting a potential therapeutic strategy for its treatment. - Source: PubMed
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Zhang ZhiguangWu OuqiangYing JiahaoJin YuxinWang HuiTian HaijunChen QizhuChen LinjieTao ChenLou ChaoJones MorganWang XiangyangMakvandi PooyanShen ShuyingLi BinWu Aimin