Mahira Muhamadeari

Biotechnology researcher with extensive experience in cell biology, molecular biology, flow cytometry, and immunology. Specialized in HL-60 neutrophil differentiation, immune response studies, and β-cell function in diabetes research. Proficient in experimental design, cell-based assays, immunostaining, and data analysis. Passionate about advancing scientific understanding in the fields of immunology, biotechnology, and diabetes.

Accomplishments

Conference Presentations & Participation

• 2015 – Presented research at the Japanese Diabetes Society Conference, Shimonoseki, Japan

• 2016 – Attended the German Diabetes Society Conference, Germany

• 2016 – Participated in the Incretin Research Meeting, Japan

• 2018 – Presented research at the Japanese Diabetes Society Conference, Japan

Research & Scientific Contributions

In 2015, I presented my research at the 58th Annual Meeting of the Japan Diabetes Society held in Shimonoseki, Japan. My study focused on the development and characterization of new clonal pancreatic β-cell lines, specifically MIN6-K8 and MIN6-K20, to investigate incretin hormone signaling and insulin secretion mechanisms.

Key Aspects of My Research:

• MIN6-K8 and MIN6-K20 Cell Lines: These cell lines were established from the IT6 mouse model, which develops insulinoma. MIN6-K8 cells respond to glucose and incretins like GLP-1 and GIP, while MIN6-K20 cells respond to glucose but not to these incretins.

• Incretin Responsiveness: I explored how incretins influence insulin secretion in these cell lines. Interestingly, forming pseudoislets from MIN6-K20 cells induced incretin responsiveness, highlighting the role of cell-cell interactions in β-cell function.

• Pseudoislet Formation: By culturing MIN6-K20 cells to form pseudoislets, I observed that this configuration restored incretin responsiveness, offering a valuable model to study β-cell behavior and signaling pathways.

This work provides insights into β-cell function and the mechanisms underlying incretin-induced insulin secretion, contributing to our understanding of diabetes pathophysiology.

“Inhibition of SNAT5 Induces Incretin-Responsive State From Incretin-Unresponsive State in Pancreatic β-Cells: Study of β-Cell Spheroid Clusters as a Model”

Authors: Mahira Hashim, Norihide Yokoi, Harumi Takahashi, Ghupurjan Gheni, Oduori S. Okechi, Tomohide Hayami, Naoya Murao, Shihomi Hidaka, Kohtaro Minami, Akira Mizoguchi, Susumu Seino

Published in: Diabetes, 2018; 67(9):1795–1806

DOI: 10.2337/db17-1486

PubMed: 29954738

“Please note that my name on this publication appears as Mahira Hashim, which was my name prior to becoming a Japanese citizen. After my graduation, my family and I adopted a new family name in accordance with Japanese regulations. My current name is Mahira Muhamadeari.”