Skip To Main Content
Zhinan Yin on Muck Rack

Zhinan Yin

As seen in: Color Research & Application, Nature, Molecular Cancer, Cell Reports, Canadian Journal of Infectious Diseases & Medical Microbiology
Is this you? As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work. Claim your profile

Get in touch with Zhinan

Contact Zhinan, search articles and posts on X, monitor coverage, and track replies from one place.

Learn more about Muck Rack

Actions

Share this page

Is this you?

As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
Claim your profile

Articles

Metformin sensitizes esophageal squamous cell carcinoma to Vγ9Vδ2 T cell-mediated cytotoxicity by upregulating BTN3A1 and BTN2A1

|
By Zishan Yang, Yadi Liu, Yixuan Han, Lijun Tan, Suli Wang, Shenglan Zhang, Chenyang Li, Yaxin Zhang, Zhinan Yin, Jian Li, Feng Ren, Piaoyi He, Yilong Ji
| Nature Verified
Abstact Metformin, a first-line anti-diabetic agent, exhibits broad-spectrum antitumor properties, though its underlying immunomodulatory mechanisms remain incompletely characterized. Here, we demonstrate that metformin significantly upregulates BTN3A1 and BTN2A1 expression on esophageal cancer cells in an AMPK-dependent manner, thereby sensitizing them to Vγ9Vδ2 T cell-mediated cytotoxicity.
Open in Who Shared Issue with article?

Immunological synapse: structures, molecular mechanisms and therapeutic implications in disease - Signal Transduction and Targeted Therapy

|
By Zhinan Yin, Le Li
| Nature Verified
Abstract The immunological synapse (IS) serves as the fundamental architectural framework for direct interactions and secretory crosstalk between immune cells, as well as between immune cells and other cells. Its dysregulation is thought to be a key underlying cause of immune evasion or inflammation observed in various diseases, including tumors and infections.
Open in Who Shared Issue with article?

KLHL25-ACLY module functions as a switch in the fate determination of the differentiation of iTreg/Th17 - Communications Biology

|
By Miaomiao Tian, Fengqi Hao, Xin Jin, Yang Wang, Yunpeng Feng, Dan Li, Zhinan Yin, Xueqing Ba
| Nature Verified
Abstract The differentiation of Th17 and iTreg is tightly associated with fatty acid metabolism. TGFβ1-induced iTreg differentiation from Th0 relies on fatty acid oxidation (FAO), whereas IL-6 with TGFβ1 shifts metabolism to Th17-preferred fatty acid synthesis (FAS). However, how IL-6 reprograms fatty acid metabolism remains unclear. Here, we unveiled that TGFβ1-activated JNK is recruited to the Klhl25 promoter by NF-YA.
Open in Who Shared Issue with article?
See all 15 licensed articles (17 Total)