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We have previously demonstrated that a novel protein ZYG1 induces sexual cell fusion (zygote formation) of Dictyostelium cells. In the process of cell fusion, involvements of signal transduction pathways via Ca(2+) and PKC (protein kinase C) have been suggested because zygote formation is greatly enhanced by PKC activators. In fact, there are several deduced sites phosphorylated by PKC in ZYG1 protein. Thereupon, we designed the present work to examine whether or not ZYG1 is actually phosphorylated by PKC and localized at the regions of cell-cell contacts where cell fusion occurs. These were ascertained, suggesting that ZYG1 might be the target protein for PKC. A humanized version of zyg1 cDNA (mzyg1) was introduced into myoblasts to know if ZYG1 is also effective in cell fusion of myoblasts. Quite interestingly, enforced expression of ZYG1 in myoblasts was found to induce markedly their cell fusion, thus strongly suggesting the existence of a common signaling pathway for cell fusion beyond the difference of species.
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http://dx.doi.org/10.1155/2012/657423 | DOI Listing |
Future Oncol
September 2025
Division of Leukemia, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL) is characterized by the fusion gene which produces a constitutively active tyrosine kinase which drives disease pathogenesis and is associated with resistance to conventional chemotherapy. Intensive cytotoxic chemotherapy followed by allogeneic hematopoietic stem cell transplantation (HSCT), the historical treatment paradigm for Ph+ ALL, was associated with poor outcomes. The introduction of inhibitors of ABL1 revolutionized the treatment of Ph+ ALL.
View Article and Find Full Text PDFCancer Treat Res Commun
September 2025
Department of Oncology, Aarhus University Hospital (AUH), Palle Juul-Jensens Blvd. 99, 8200 Aarhus N (DK), Denmark.
Purpose: We investigated whether EML4-ALK fusions and mutations in pre-treatment plasma ctDNA predicted time to treatment discontinuation (TTD) in ALK-positive non-small cell lung cancer (ALK+ NSCLC) patients initiating first-line alectinib and evaluated clinical characteristics influencing TTD.
Materials & Methods: 42 patients from five Danish public oncology departments with previously untreated, metastatic ALK+ NSCLC were included in the study. All patients received alectinib, a second-generation ALK inhibitor, as their first-line treatment.
Dev Biol
September 2025
Department of Biological Sciences, University of Denver, Denver, CO 80208, USA; Department of Biochemistry and Biophysics, AgriLife Research, Texas A&M University, College Station, TX 77843, USA. Electronic address:
During fertilization, sperm and egg membranes signal and fuse to form a zygote and begin embryonic development. As lipids participate in signaling and membrane fusion, we investigated the role of lipid asymmetry in gametogenesis, fertilization, and embryogenesis. We show that the lipid flippase TAT-5, an essential P4-ATPase that maintains phosphatidylethanolamine asymmetry, is required for both oocyte formation and sperm activation, albeit at different levels of flippase activity.
View Article and Find Full Text PDFBioessays
September 2025
Department of Biological Sciences, Tata Institute of Fundamental Research, Mumbai, India.
The timely release of chemical messengers is a crucial step in cell-to-cell communication. Does this release occur as a passive diffusion from the donor membrane or it is actively regulated? A series of studies indicated that chemical messengers' secretion is "sub-quantal". This mode of secretion demands a strongly regulated release mechanism and calls for a thorough characterization of the release sites.
View Article and Find Full Text PDFBioorg Chem
September 2025
Department of Pharmacy, Personalized Drug Research and Therapy Key Laboratory of Sichuan Province, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China. Electronic address:
RET tyrosine kinase, a key regulator of cellular signaling, is abnormally activated due to mutations or fusions in various cancers, making it an important therapeutic target. Traditional multi-kinase inhibitors (MKIs, such as cabozantinib and vandetanib) exhibit significant side effects due to non-selective inhibition of targets like VEGFR, and also suffer from resistance associated with RET mutations (e.g.
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