PDGFRB & PTPN11 Protein Protein Interaction Antibody Pair
- Known as:
- PDGFRB & PTPN11 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0034
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- PDGFRB & PTPN11 Protein Interaction Antibody Pair
Related genes to: PDGFRB & PTPN11 Protein Protein Interaction Antibody Pair
- Gene:
- PDGFRB NIH gene
- Name:
- platelet derived growth factor receptor beta
- Previous symbol:
- PDGFR
- Synonyms:
- JTK12, CD140b, PDGFR1
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
- Gene:
- PTPN11 NIH gene
- Name:
- protein tyrosine phosphatase non-receptor type 11
- Previous symbol:
- NS1
- Synonyms:
- BPTP3, SH-PTP2, SHP-2, PTP2C, SHP2
- Chromosome:
- 12q24.13
- Locus Type:
- gene with protein product
- Date approved:
- 1993-03-03
- Date modifiied:
- 2019-04-23
Related products to: PDGFRB & PTPN11 Protein Protein Interaction Antibody Pair
Related articles to: PDGFRB & PTPN11 Protein Protein Interaction Antibody Pair
- Bisphenol A (BPA), a prototypical environmental endocrine-disrupting chemical (EDC), is ubiquitously present in environmental matrices and biological fluids. Dietary ingestion and inhalation exposure to BPA can induce testicular oxidative stress and apoptosis. This study aimed to investigate the protective effects and underlying mechanisms of (Pg), a perennial herb of the Amaranthaceae family, against BPA-induced reproductive system injury. Potential targets and molecular mechanisms were predicted through network pharmacology. Physiological indicators, histopathological changes, serum biochemical parameters, and Western blot analysis were used to systematically evaluate the ameliorative effects of Pg and elucidate its mechanisms. Our network pharmacology analysis identified core targets of Pg in attenuating reproductive system injury, including PTPN11, PIK3CA, JAK2, PIK3R1, PDGFRB, and others. GO enrichment and KEGG pathway analysis indicated that these key targets primarily regulate steroid metabolism, enhance antioxidant capacity, and modulate signaling pathways such as PI3K-AKT, Fc epsilon RI, and cAMP. In vivo studies demonstrated that all Pg dose groups showed significant improvement in BPA-induced histopathological injury to testicular tissues. BPA exposure increased serum levels of follicle-stimulating hormone (FSH) while decreasing testosterone (T), estradiol (E2), and progesterone (PROG) levels. Furthermore, BPA elevated serum levels of the testicular marker enzymes acid phosphatase (ACP) and lactate dehydrogenase (LDH) but reduced alkaline phosphatase (ALP) levels; all these effects were significantly reversed with Pg treatment. Western blot results showed that compared with the model group, high-dose Pg significantly upregulated the expression of phosphorylated AKT (p-AKT), phosphorylated PI3K (p-PI3K), and Bcl-2, while downregulating Cleaved Caspase-3 and Bax. Our findings indicate that Pg may attenuate BPA-induced reproductive system injury by activating the PI3K/AKT signaling pathway, upregulating the anti-apoptotic protein Bcl-2, and inhibiting the activation of the apoptotic effector Caspase-3. The study provides a new theoretical basis for the development of novel natural drugs or health products. - Source: PubMed
Publication date: 2025/10/25
Xue HongweiZhang ShuyanLu JuanLiu JiaLi YihangChen Xi - Sivelestat is a specific neutrophil elastase inhibitor that is currently approved for the treatment of acute lung injury and acute respiratory distress syndrome. Given sivelestat's established anti-inflammatory and antioxidant properties, its efficacy in treating pulmonary arterial hypertension (PAH) remains uncertain. This study aims to investigate the potential of sivelestat as a treatment for PAH. - Source: PubMed
Publication date: 2025/05/20
Deng XiaodongQiu PengchengLi XinHu YukunQue QingZhang KunchiDeng TianlinLiu Yi - Resistance in anti-cancer treatment is a result of clonal evolution and clonal selection. In chronic myeloid leukemia (CML), the hematopoietic neoplasm is predominantly caused by the formation of the BCR::ABL1 kinase. Evidently, treatment with tyrosine kinase inhibitors (TKIs) is tremendously successful. It has become the role model of targeted therapy. However, therapy resistance to TKIs leads to loss of molecular remission in about 25% of CML patients being partially due to BCR::ABL1 kinase mutations, while for the remaining cases, various other mechanisms are discussed. - Source: PubMed
Publication date: 2023/06/13
Kaehler MeikeOsteresch PiaKünstner AxelVieth Stella JulianeEsser DanielaMöller MariusBusch HaukeVater IngaSpielmann MalteCascorbi IngolfNagel Inga - Disruption of fetal membranes before the onset of labor is referred to as premature rupture of membranes (PROM). Lack of maternal folic acid (FA) supplementation reportedly leads to PROM. However, there is a lack of information on the location of FA receptors in the amniotic tissue. Additionally, the regulatory role and potential molecular targets of FA in PROM in vitro have rarely been investigated. - Source: PubMed
Publication date: 2023/04/18
Lee Ah-YoungKong DeqiCho HeeryunChoi EunsaemHwang SoowonSong YuniChoi Ehn-KyoungKim Yun-BaeGeum Dong HoKim Ho YeonCho Geum JoonAhn KihoonOh Min-JeongKim Hai-JoongHong Soon-Cheol - Malignant peripheral nerve sheath tumors often arise in patients with neurofibromatosis type 1 and are among the most treatment-refractory types of sarcoma. Overall survival in patients with relapsed disease remains poor, and thus novel therapeutic approaches are needed. NF1 is essential for negative regulation of RAS activity and is altered in about 90% of malignant peripheral nerve sheath tumors (MPNST). A complex interplay of upstream signaling and parallel RAS-driven pathways characterizes NF1-driven tumorigenesis, and inhibiting more than one RAS effector pathway is therefore necessary. To devise potential combination therapeutic strategies, we identified actionable alterations in signaling that underlie adaptive and acquired resistance to MEK inhibitor (MEKi). Using a series of proteomic, biochemical, and genetic approaches in an model of MEKi resistance provided a rationale for combination therapies. HGF/MET signaling was elevated in the MEKi-resistant model. HGF overexpression conferred resistance to MEKi in parental cells. Depletion of HGF or MET restored sensitivity of MEKi-resistant cells to MEKi. Finally, a combination of MEK and MET inhibition demonstrated activity in models of MPNST and may therefore be effective in patients with MPNST harboring genetic alterations in . SIGNIFICANCE: This study demonstrates that MEKi plus MET inhibitor may delay or prevent a novel mechanism of acquired MEKi resistance, with clinical implications for MPNST patients harboring alterations. - Source: PubMed
Publication date: 2020/11/17
Wang JiawanPollard KaiCalizo AnaPratilas Christine A