TRPM7 activity drives human CD4 T-cell activation and differentiation in a magnesium dependent manner.

T lymphocyte activation is a crucial process in the regulation of innate and adaptive immune responses. The ion channel-kinase TRPM7 has previously been implicated in cellular Mg homeostasis, proliferation, and immune cell modulation. Here, we show that pharmacological and genetic silencing of TRPM7 leads to diminished human CD4 T-cell activation and proliferation following TCR mediated stimulation.

Transient Receptor Potential Melastatin 7 (TRPM7) Ion Channel Inhibitors: Preliminary SAR and Conformational Studies of Xenicane Diterpenoids from the Hawaiian Soft Coral .

Waixenicin A, a xenicane diterpene from the octocoral , is a selective, potent inhibitor of the TRPM7 ion channel. To study the structure-activity relationship (SAR) of waixenicin A, we isolated and assayed related diterpenes from . In addition to known waixenicins A () and B (), we purified six xenicane diterpenes, 7,8-epoxywaixenicins A () and B (), 12-deacetylwaixenicin A (), waixenicin E (), waixenicin F (), and 20-acetoxyxeniafaraunol B ().

Promoting Health Research among Underrepresented Students through the HUI SRC.

The Hawai'i Pacific University Undergraduate Infrastructure Student Research Center (HUI SRC) is focused on increasing participation of historically underrepresented populations, such as Native Hawaiians, other Pacific Islanders (NHPI), and Filipinos, in tomorrow's biomedical and health research workforce. This is achieved by promoting engagement and competency in entrepreneurial biomedical and health research among undergraduate students. The HUI SRC was modeled after the Morgan State University ASCEND SRC funded by the National Institute of General Medical Sciences.

STIM1 signals through NFAT1 independently of Orai1 and SOCE to regulate breast cancer cell migration.

Store-operated calcium entry (SOCE) contributes to several physiological and pathological conditions including transcription, secretion, immunodeficiencies, and cancer. SOCE has been shown to be important for breast cancer cell migration where knockdown of SOCE components (STIM1 or Orai1) decreases cancer metastasis. Here we show unexpectedly that complete knockout of STIM1 (STIM1-KO) using gene editing in metastatic MDA-MB-231 breast cancer cells results in faster migration and enhanced invasion capacity.