Главная > Поддержка > Справочные материалы

Справочные материалы

Receptor-Interacting Protein 3/Calmodulin-Dependent Kinase II/Proline-Rich Tyrosine Kinase 2 Pathway is Involved in Programmed Cell Death in a Mouse Model of Brain Ischaemic Stroke

Wang B, Ma L, Liu L, et al. Receptor-Interacting Protein 3/Calmodulin-Dependent Kinase II/Proline-Rich Tyrosine Kinase 2 Pathway is Involved in Programmed Cell Death in a Mouse Model of Brain Ischaemic Stroke. Neuroscience. 2022;506:14-28. doi:10.1016/j.neuroscience.2022.09.009

Рекомендуемые продукты: GAPDH покуплено у abinScience 2022-12-01
SARS-CoV-2 evolves to reduce but not abolish neutralizing action

Zhang Y, Ndzouboukou JB, Lin X, et al. SARS-CoV-2 evolves to reduce but not abolish neutralizing action. J Med Virol. 2023;95(1):e28207. doi:10.1002/jmv.28207

Рекомендуемые продукты: Research Grade Bamlanivimab Research Grade Casirivimab Research Grade lmdevimab Research Grade Etesevimab покуплено у abinScience 2022-10-19
SARS-CoV-2 evolves to reduce but not abolish neutralizing action

Zhang Y, Ndzouboukou JB, Lin X, et al. SARS-CoV-2 evolves to reduce but not abolish neutralizing action. J Med Virol. 2023;95(1):e28207. doi:10.1002/jmv.28207

Рекомендуемые продукты: Research Grade Bamlanivimab Research Grade Casirivimab Research Grade lmdevimab Research Grade Etesevimab покуплено у abinScience 2022-10-19
M6 A Modifier-Mediated Methylation Characterized by Diverse Prognosis, Tumor Microenvironment, and Immunother

Liu, F., et al. (2022). M6A modifier‑mediated methylation characterized by diverse prognosis, tumor microenvironment, and immunotherapy response in hepatocellular carcinoma. [Journal unspecified].

Рекомендуемые продукты: GAPDH покуплено у abinScience 2022-08-16
M6 A Modifier-Mediated Methylation Characterized by Diverse Prognosis, Tumor Microenvironment, and Immunother

Liu, F., et al. (2022). M6A modifier‑mediated methylation characterized by diverse prognosis, tumor microenvironment, and immunotherapy response in hepatocellular carcinoma. [Journal unspecified].

Рекомендуемые продукты: GAPDH покуплено у abinScience 2022-08-16
SEMA4D/PlexinB1 promotes AML progression via activation of PI3K/Akt signaling

Liu L, Yang L, Liu X, et al. SEMA4D/PlexinB1 promotes AML progression via activation of PI3K/Akt signaling. J Transl Med. 2022;20(1):304. Published 2022 Jul 6. doi:10.1186/s12967-022-03500-w

Рекомендуемые продукты: Anti-Human CD100/SEMA4D Antibody (SAA0331) покуплено у abinScience 2022-07-06
SEMA4D/PlexinB1 promotes AML progression via activation of PI3K/Akt signaling

Liu L, Yang L, Liu X, et al. SEMA4D/PlexinB1 promotes AML progression via activation of PI3K/Akt signaling. J Transl Med. 2022;20(1):304. Published 2022 Jul 6. doi:10.1186/s12967-022-03500-w

Рекомендуемые продукты: Anti-Human CD100/SEMA4D Antibody (SAA0331) покуплено у abinScience 2022-07-06
Evolutionarily conserved odorant-binding proteins participate in establishing tritrophic interactions

Yang, R., Li, D., Yi, S., & Wang, M. (2022). Evolutionarily conserved odorant-binding proteins participate in establishing tritrophic interactions. iScience, 25(7), Article 104664.

Рекомендуемые продукты: GAPDH покуплено у abinScience 2022-07-01
Evolutionarily conserved odorant-binding proteins participate in establishing tritrophic interactions

Yang, R., Li, D., Yi, S., & Wang, M. (2022). Evolutionarily conserved odorant-binding proteins participate in establishing tritrophic interactions. iScience, 25(7), Article 104664.

Рекомендуемые продукты: GAPDH покуплено у abinScience 2022-07-01
F‑box and WD repeat‑containing protein 7 ameliorates angiotensin II‑induced myocardial hypertrophic injury via the mTOR‑mediated autophagy pathway

Liu Q, Han C, Wu X, Zhou J, Zang W. F-box and WD repeat-containing protein 7 ameliorates angiotensin II-induced myocardial hypertrophic injury via the mTOR-mediated autophagy pathway. Exp Ther Med. 2022;24(1):464. Published 2022 May 23. doi:10.3892/etm.2022.11391IF: 2.4 Q3

Рекомендуемые продукты: Anti-Human NPPA Polyclonal Antibody покуплено у abinScience 2022-05-23

Получить бесплатный расчет