PAK2 pSer197 antibody Ab
- Known as:
- PAK2 pSer197 (anti-) Antibody
- Catalog number:
- 1488163
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- PAK2 pSer197 antibody
Related genes to: PAK2 pSer197 antibody Ab
- Gene:
- PAK2 NIH gene
- Name:
- p21 (RAC1) activated kinase 2
- Previous symbol:
- -
- Synonyms:
- PAK65, PAKgamma
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-25
- Date modifiied:
- 2016-10-24
Related products to: PAK2 pSer197 antibody Ab
Related articles to: PAK2 pSer197 antibody Ab
- Mycotoxin contamination in the food chain poses serious risks to human and animal health, and aflatoxin B1 (AFB1) is the most toxic and carcinogenic compound Advanced strategies for mycotoxin mitigation emphasize biological control using non-pathogenic microorganisms. This study presents the first report of isolating Metschnikowia pulcherrima in Pakistan and its novel application as a biocontrol agent against AFB1. Three strains of M. pulcherrima, pak2 (MW341425), pak3 (MW341426), and pak4 (MW341427), were isolated from fruits (apple, orange, guava, and grape) using the dilution plate technique and evaluated for AFB1-binding potential using whole cells, cell walls, and glucan extracts. From a 100mL culture, 400 mg of yeast biomass produced 35 mg glucan and 5 mg chitin (cell wall proxy). AFB1 was produced and purified from Aspergillus flavus and quantified by HPLC. Binding assays were conducted by incubating 140ppb AFB1 with yeast components at 25 °C under agitation (200 rpm) for 0.5, 1, and 2 h. The highest AFB1 binding was achieved by M. pulcherrima pak3 whole cells (77.37 ± 1.48%) after 1 h Interaction time. Glucan extracts from M. pulcherrima pak3 and M. pulcherrima pak4 showed strong binding (74.99 ± 2.14) within 1-2 h of interaction. However, cell wall fractions showed lower efficacy as compared to glucan component. The cell wall of M. pulcherrima pak4 showed maximum binding (54.28 ± 2.86%) after 2 h. Results indicate that M. pulcherrima, particularly its whole cells and glucan components, effectively bind AFB1 in In-vitro assay suggesting its potential as a natural AFB1 mitigation tool in food and feed. This work highlights the importance of indigenous yeast strains in enhancing food safety. - Source: PubMed
Publication date: 2026/07/02
Sana SabaKhan AyeshaKhan Qaiser FaridNazir LayyabaElhajji Feras DarwishSiddiqui Muhammad AliShehzad UsmanIqbal Muhammad SarfarazSaid Musa ABabakarkhil TariqDawoud Turki M - Vasculo-Behcet disease (VBD) is a complex form of systemic vasculitis with an unclear etiology. It is believed to arise from a combination of immune dysregulation, genetic susceptibility, and epigenetic influences. The disease can be life-threatening due to severe vascular complications such as occlusions, thrombosis, and aneurysm formation. This study aimed to explore the relationship between clinical manifestations and genetic findings in a patient with VBD from Pakistan, where awareness and genetic research on this condition remain limited. Five patients with clinically confirmed VBD were evaluated, and whole exome sequencing (WES) was performed in one patient to investigate potential disease-associated variants. All patients showed evidence of vascular inflammation. Cerebral venous sinus thrombosis (CVST) was observed in three patients, while aneurysm, ST, venous stasis ulcer, and stroke were each identified in two. One patient presented with venous stasis thrombosis together with pulmonary and non-pulmonary arterial thrombosis and macroangiopathic ischemic changes. WES identified nineteen rare nonsynonymous variants (minor allele frequency < 1%) across nineteen genes. Phenotype-based database analysis identified four genes - DPEP1, DNAH5, RHOD, and LRP2 - with reported associations with vascular disorders. Pathway enrichment analysis using ClueGO highlighted seven genes - PAK2, RHOD, MST1, NPHS1, STAR, SLC25A5, and LRP2. Together, these analyses prioritized nine candidate genes with potential relevance to vascular pathology in VBD. Notably, variants in DPEP1 (c.750 C > G, p.Asp250Glu), DNAH5 (c.4807 C > A, p.Pro1603Thr), RHOD (c.244 C > T, p.Arg82Trp), and LRP2 (c.2636G > C, p.Trp879Ser) corresponded to the vascular manifestations observed in our patients, including thrombosis and vessel inflammation. As WES was performed in only one patient, these genetic findings should be considered exploratory. Nevertheless, the results provide preliminary insight into the genetic background of VBD in the Pakistani population and highlight candidate genes that warrant further investigation in larger patient cohorts. - Source: PubMed
Publication date: 2026/07/01
Waqas AyeshaYasmin AzraWatson Christopher MarkAhmed IbrarSavic Sinisa - Trophoblastic cell migration is essential for the attachment of the placenta to uterine wall, which is a critical step for fetal development. Aberrant migration of trophoblastic cells can lead to pregnant pathologies such as preeclampsia (PE), while the molecular mechanisms remain largely unknown. The current study investigated the effects and molecular mechanisms of the HAND1-Rac1-PAK axis in trophoblast migration using the HTR-8/SVneo cell line, isolated human primary cytotrophoblasts, and human placental tissues. We report herein that HAND1 is highly expressed in human early placenta and promotes trophoblastic cell migration. Mechanistically, HAND1 potentiates human trophoblastic cell migration via activating Vav2/Rac1/PAKs signaling, and the elevated capacity of HAND1 in inducing migration is dependent on its Serine/Threonine phosphorylation status, which is reciprocally regulated by PAK2 and is directly associated with the subsequent degradation of HAND1 protein, thereby generating a positive feed-back for HAND1-mediated trophoblasts migration during human pregnancy. The data suggest that HAND1 is essential for regulating human trophoblast function, potentially enhancing our understanding of pregnancy maintenance and contributing to new therapies for gestational disorders. - Source: PubMed
Publication date: 2026/06/26
Ye WeifengZhu ChongyingBao YiyaoLi LinAn ZihaoSong YanXu QiangJin MeiyuanTang Chao - 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), a dietary heterocyclic amine generated during high-temperature cooking, has been implicated in colorectal cancer (CRC); however, its underlying molecular mechanisms remain incompletely understood. In this study, we provide experimental evidence that PhIP induces proliferative and oxidative stress-related responses in colorectal cancer cells through a PAK2-dependent mechanism. In vitro assays demonstrated that PhIP exposure robustly enhanced colorectal cancer cell proliferation in both time- and concentration-dependent manners and induced marked redox imbalance, as evidenced by decreased HO-1 expression and concomitant upregulation of catalase (CAT) and SOD2. Critically, siRNA-mediated knockdown of PAK2 significantly abrogated PhIP-induced proliferative effects and effectively reversed oxidative stress-related alterations, establishing PAK2 as a functional mediator rather than a passive biomarker. Consistently, in vivo xenograft experiments further demonstrated that PAK2 silencing markedly suppressed colorectal tumor growth, supporting a general tumor-promoting role of PAK2 rather than directly demonstrating PhIP-induced carcinogenesis in vivo. Mechanistically, integrative analyses combining network toxicology, Mendelian randomization, multi-omics profiling, and molecular docking prioritized PAK2 as a candidate hub gene potentially connecting PhIP-related targets with CRC-associated molecular features and supported a stable binding pattern between PhIP and PAK2 in silico. Functional enrichment analyses further indicated that PAK2-associated signatures are involved in oxidative stress, mitochondrial metabolism, and cell cycle regulation. Collectively, these findings support PAK2 as a functional mediator of PhIP-induced cellular responses in colorectal cancer cells, while the in vivo data demonstrate the broader role of PAK2 in colorectal tumor growth. - Source: PubMed
Publication date: 2026/06/11
Li ZeliXie DongxuTao WangWu XinyanZhang GeFu Jiarui NicoleLi ShuwenCai Shanshan - BRAF fusions are rare but recurrent driver events in a spectrum of mostly pediatric and young adult mesenchymal soft tissue tumors, including infantile fibrosarcoma, lipofibromatosis-like neural tumors, and other kinase fusion spindle cell neoplasms. Their clinicopathologic spectrum, co-occurring secondary genomic events, and frequency among various sarcoma histotypes remain incompletely characterized. The purpose of this study is to comprehensively investigate the incidence and structural variants of BRAF fusions among a large clinicopathologic and molecular sarcoma cohort. The additional goal was to distinguish primary driver BRAF fusions from potential passenger events and correlate with sarcoma histotypes. We identified a total of 24 cases harboring BRAF fusions, with 18 (75%) occurring in canonical BRAF-driven histotypes, including kinase-associated spindle cell tumors (n = 12), myxoinflammatory fibroblastic sarcoma (n = 3), GIST (n = 2) and one hybrid nerve sheath tumor. The remaining six cases were detected in various established pathologic entities (undifferentiated pleomorphic sarcoma, angiosarcoma, embryonal rhabdomyosarcoma, dedifferentiated liposarcoma, PEComa), likely as secondary or passenger events. Among the 12 kinase-associated spindle cell tumors, the most common histologies included tumors resembling infantile fibrosarcoma (n = 4), malignant peripheral nerve sheath tumor (n = 3), lipofibromatosis (n = 2), and myoid/pericytic lesions (n = 2). This predominant group had a wide age range at diagnosis (median 15.5 years), a predilection for soft tissues of extremities, trunk, and head/neck and showed CD34 and S100 co-expression in 45% of cases. In this group, BRAF breakpoints clustered in exons 8-11 retaining an intact kinase domain, and fusion partners were diverse (AGK, AHNAK, NRF1, PAK2, TMEM245, FNBP1, STEAP4, TSC1, KIAA1549). Tumor mutation burden was consistently low, with CDKN2A homozygous deletion being the only recurrent secondary event (4/5 cases profiled). Among the five patients with follow-up (median 34 months), one patient died of disease, with two developing local recurrences at 5 and 84 months. The BRAF fusions occurring in non-canonical histotypes had similar breakpoint patterns and various partners. These results highlight the heterogeneity of mesenchymal neoplasms harboring BRAF fusions, including both driver and likely secondary genetic events, which often require a comprehensive approach that integrates clinical, histopathologic, and detailed molecular data, for a definitive classification. - Source: PubMed
Yeung Maximus C FAntonescu Cristina R