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In0.17Al0.83N/GaN high‐electron‐mobility transistor (HEMT) using GaN‐on‐Insulator (GaNOI) technology via 200 mm wafer bonding technique is developed with good DC and RF performance and high fT/fmax. Measurements obtained from X‐Ray diffraction and micro‐Raman spectroscopy have demonstrated a 5% reduction in "a lattice strain," which results in the improvement of the sheet resistance (Rsh) from 301 to 284 Ω □−1. A 120 nm gate‐length device achieves a peak fT up to 96 GHz which yields a fT × Lg value of 11.5 GHz μm, which compares favorably with reported GaN‐based HEMTs on Si. These results demonstrate that GaNOI HEMT on Si is an attractive candidate for future mm‐wave applications. The implementation of GaNOI technology facilitates the integration of GaN devices into a chip alongside complementary metal–oxide–semiconductor technology that opens up the potential for integrated high‐power and RF applications, enabling more compact and efficient systems. [ABSTRACT FROM AUTHOR]

This work investigates the off-state leakage characteristics of AlN/GaN/AlGaN high electron mobility transistors (HEMTs) on Si substrate with varying mesa depths and uncovers the existence of a parasitic channel associated with the AlGaN back barrier. Significant differences in off-state leakage up to three orders of magnitude were observed between devices fabricated using different mesa depths. The electrical properties of AlN/GaN/AlGaN HEMTs were measured, and it was found that there is a N-type parasitic channel in the unintentionally doped AlGaN back-barrier. Analysis of the isolation test structure, which retains this parasitic channel, reveals a buffer leakage of 12.8 mA/mm and a sheet resistance of 7739.1 Ω/sq, as a result of the parasitic channel. The depletion electric field strength of the parasitic channel is 3.2 × 105 V/cm. Temperature-dependent I–V curves obtained from the isolation area affirm that the primary leakage mechanism is two-dimensional variable range hopping along the sidewall. As the isolation distance extends from 3 to 5 μm, the slope of the fitting line decreases from −53.14 to −126.11 due to increased resistance. [ABSTRACT FROM AUTHOR]

N-p-n InGaP/GaAs double heterojunction bipolar transistor has been successfully grown on a 200 mm Ge/Si wafer using metalorganic chemical vapor deposition with low defect density of 107 cm-2. Non-gold metals of Ni/Ge/Al and Ti/Al are used to form the ohmic contact for small pieces device fabrication. Both direct-current (dc) and high-frequency characteristics of the device were measured. The device with emitter area of 6 × 8 μm2 shows a dc gain of 55 at a collector current of Ic = 4 mA, with high collector-emitter breakdown voltage of ~17 V. The high-frequency response with cutoff frequency (fT) of 23 GHz and maximum available frequency (fmax) of 10 GHz can be achieved. These results demonstrate that InGaP/GaAs double heterojunction bipolar transistor grown on low defect density Ge/Si wafer has the potential for realizing III-V CMOS integrated platform for high-frequency applications.

Simple Summary: N7-methylguanosine (m7G) methylation plays an important role in the development of pancreatic adenocarcinoma (PDAC). Among the 29 regulatory genes of m7G methylation, they can be roughly divided into three categories: methyltransferase (writer), demethylase (eraser), and binding protein (reader) according to their functions. In this study, we explore the role of m7G reader NCBP2 in PDAC progression: NCBP2 activates MEK/ERK signaling by upregulating c-JUN, thereby promoting PDAC cell proliferation. In summary, we identify a novel potential therapeutic target for PDAC, which sheds new light on the treatment of PDAC patients. PDAC is one of the most common malignant tumors worldwide. The difficulty of early diagnosis and lack of effective treatment are the main reasons for its poor prognosis. Therefore, it is urgent to identify novel diagnostic and therapeutic targets for PDAC patients. The m7G methylation is a common type of RNA modification that plays a pivotal role in regulating tumor development. However, the correlation between m7G regulatory genes and PDAC progression remains unclear. By integrating gene expression and related clinical information of PDAC patients from TCGA and GEO cohorts, m7G binding protein NCBP2 was found to be highly expressed in PDAC patients. More importantly, PDAC patients with high NCBP2 expression had a worse prognosis. Stable NCBP2-knockdown and overexpression PDAC cell lines were constructed to further perform in-vitro and in-vivo experiments. NCBP2-knockdown significantly inhibited PDAC cell proliferation, while overexpression of NCBP2 dramatically promoted PDAC cell growth. Mechanistically, NCBP2 enhanced the translation of c-JUN, which in turn activated MEK/ERK signaling to promote PDAC progression. In conclusion, our study reveals that m7G reader NCBP2 promotes PDAC progression by activating MEK/ERK pathway, which could serve as a novel therapeutic target for PDAC patients. [ABSTRACT FROM AUTHOR]