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Molecular Imaging in Individualized Cancer Management
Published in Brian Leyland-Jones, Pharmacogenetics of Breast Cancer, 2020
David M. Schuster, Diego R. Martin
Apoptosis, or programmed cell death, is an elementary process of life that maintains homeostasis. Apoptosis is physiologic and is different from necrosis, which is pathologic, often eliciting an inflammatory reaction. Successful chemotherapy increases apoptosis and enhances the uptake of annexin in the tumor. As the tumor becomes necrotic, the uptake of annexin reduces. PET and SPECT imaging with radiolabeled annexin have been used to assess apoptosis (58–61).
The Etiology of the Antiphospholipid Syndrome
Published in Howard J.A. Carp, Recurrent Pregnancy Loss, 2020
Sara De Carolis, Giuseppina Monteleone, Cristina Garufi, Rotem Inbar, Miri Blank, Yehuda Shoenfeld
Furthermore, aPL may influence the placental circulation by attacking certain placental epitopes such as Annexin A5, a potent anticoagulant protein. Annexin V, found on the apical surface of placental syncytiotrophoblast, forms a protective shield on the phospholipid surface, blocking phospholipids from becoming available for coagulation reactions. The annexin-V shield could be damaged by either binding to anti-annexin-V or preventing its binding to the PL membrane, or by blocking autoantibodies against annexin-V/PL [36]. Anti-annexin-V autoantibodies have been detected in patients with systemic lupus erythematosus (SLE) and APS associated with pregnancy loss, while reduced levels of annexin-V have been observed on the placental villi of women with aPL, recurrent pregnancy loss, and a thrombogenic background [37].
Golgi apparatus regulation of differentiation
Published in C. Yan Cheng, Spermatogenesis, 2018
Louis Hermo, Regiana L. Oliveira, Charles E. Smith, Catherine E. Au, John J. M. Bergeron
Annexin A6 is a calcium-dependent membrane binding protein linked to membrane and cytoskeletal organization and cholesterol homeostasis.121 It may serve a function in membrane trafficking122 that is highly active in acrosome formation.
High fragmentation in platelet concentrates impacts the activation, procoagulant, and aggregatory capacity of platelets
Published in Platelets, 2023
Nahreen Tynngård, Aseel Alshamari, Per Sandgren, Dermot Kenny, Ana Maria Vasilache, Mohammad R. Abedi, Sofia Ramström
To address this, we studied PCs with different initial compositions in regard to platelet fragmentation and its impact on storage-induced changes in activation potential. A novel flow cytometry protocol was used, which simultaneously evaluates five important platelet functions described below. PAC-1 binds to the active conformational form of the fibrinogen receptor GPIIb/IIIa, necessary for platelet aggregation [6]. Annexin V binds to phosphatidylserine (PS), needed for assembly of the prothrombinase complex on platelets. Loss of DiIC1(5) staining indicates decreased mitochondrial membrane potential as occurs in procoagulant platelets [7]. P-selectin and LAMP-1 exposures are signs of α-granule release and lysosomal exocytosis, respectively [8]. Furthermore, the protocol allows for the analysis of platelet subpopulations, e.g., normal-sized platelets, the formation of smaller, procoagulant platelets, and platelet fragments (microparticles), which normally appear following strong stimulation of the platelets [9]. Furthermore, aggregation capacity and release of soluble platelet activation markers were determined.
Insights into the activation of oral keratinocyte cell death by Candida albicans and Staphylococcus aureus biofilms
Published in Biofouling, 2021
Kassia de Carvalho Dias, Paula Aboud Barbugli, Carlos Eduardo Vergani
The induction of apoptosis was assessed using fluorescence staining cells with Hoechst 33342, annexinV/Alexa Fluor 488 and (PI) Propidium Iodide (Molecular Probes, Invitrogen, Maryland, USA). Annexin V binds specifically to the phosphatidylserine residue on the cell membrane during apoptosis. PI intercalates into the damaged DNA, a typical consequence of cell necrosis or late apoptosis (Leist and Nicotera 1997; Hu et al. 2009). After overnight contact with the single and dual biofilms SF, the NOK-si cells were washed twice with binding buffer (10 mM Hepes/NaOH, 140 mM NaCl, 2.5 mMCaCl2, pH = 7.4) and incubated with Hoechst (1.5 μl ml−1), annexinV (10 μl well−1) and PI 2 μl (100 μg ml−1) for 20 min at room temperature. Thereafter, the cells were washed with PBS. The counting of apoptotic/necrotic cells was performed using the InCell Analyzer 2000 (GE Healthcare, Salt Lake City, Utah, USA) and the Quantify Image Analysis Software package (GEHealthcare, Salt Lake City, Utah, USA).
Multi-omics reveals novel prognostic implication of SRC protein expression in bladder cancer and its correlation with immunotherapy response
Published in Annals of Medicine, 2021
Wenhao Xu, Aihetaimujiang Anwaier, Chunguang Ma, Wangrui Liu, Xi Tian, Maierdan Palihati, Xiaoxin Hu, Yuanyuan Qu, Hailiang Zhang, Dingwei Ye
This study first identified landscape of novel prognostic protein signatures in the discovering dataset based on large-scale RPPA data (n = 340). Next, potential integrated prognosis-related proteins (IPRPs) model (including BECLIN, PKCALPHA, EGFR, ANNEXIN1, AXL and SRC) was constructed to assess the survival risk score of bladder cancer. BECLIN is identified as a necessary autophagy protein, which has been proved to play an essential role in BECLIN ± mice tumour inhibition [42]. PKCALPHA involved in mediating cell proliferation, differentiation and apoptosis. In the process of cell function regulation, it interacts with many proto-oncogenes [43]. The expression and activation of EGFR are related to many precancerous lesions and malignant tumours [44], and is associated with malignancy of at least 33–50% of human epithelial tumours [45]. In addition, EGFR has been considered to be the carcinogenic driver of NSCLC and predicts TKI inhibitors therapy responses [46]. ANNEXIN1 is a member of the ANNEXIN protein superfamily, which not only has a very clear anti-inflammatory effect, but also plays an important role in apoptosis [47]. Importantly, ANNEXIN1 has been proved to be a key regulator of adaptive immunity through its ability to control T cell activation and autoimmune diseases [48]. Next, the overexpression of AXL is found closely related to cell proliferation, migration and invasion by activating carcinogenic signalling pathways, including PI3K/Akt and/or MAPK/Erk [49].