Kinases: MINK1 , protein, Expression system: Sf9 cells
- Known as:
- Kinases: MINK1 , protein, Expression system: Sf9 cells
- Catalog number:
- PK-MINK1-A010
- Product Quantity:
- 10
- Category:
- -
- Supplier:
- BIaff
- Gene target:
- Kinases: MINK1 protein Expression system: Sf9 cells
Related genes to: Kinases: MINK1 , protein, Expression system: Sf9 cells
- Gene:
- MINK1 NIH gene
- Name:
- misshapen like kinase 1
- Previous symbol:
- -
- Synonyms:
- B55, MINK, ZC3, MAP4K6, YSK2
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-20
- Date modifiied:
- 2016-04-04
Related products to: Kinases: MINK1 , protein, Expression system: Sf9 cells
Related articles to: Kinases: MINK1 , protein, Expression system: Sf9 cells
- Symptom heterogeneity in atrial fibrillation (AF) remains poorly understood, and its biological basis, including genetic influences, is unclear. - Source: PubMed
Publication date: 2026/07/20
Okamura ShoFurutani MotokiNakashima MikaOda NoboruTokuyama TakehitoOkubo YousakuMiyauchi ShunsukeMiyamoto ShogoOguri NaotoSakai TakumiIshibashi NaokiMaeda JunjiIshida ShunsukeNiida ShumpeiOzaki KouichiShigemizu DaichiOchi HidenoriNakano Yukiko - Astrocytes are a subset of glial cells in the central nervous system (CNS) that support numerous processes essential for brain function. Their functional diversity is thought to arise from specialized subpopulations with distinct molecular profiles. Although single-cell and single-nucleus RNA sequencing (scRNA-seq and snRNA-seq) have greatly advanced our understanding of astrocyte transcriptomic heterogeneity, mRNA abundance does not always correlate with protein levels because of post-transcriptional and translational regulation. Therefore, studying protein profiles remains essential to accurately capture astrocyte functional states and heterogeneity. Here, we used Microscoop Mint, a microscopy-guided spatial proteomics platform that integrates subcellular, region-specific sample preparation with LC-MS/MS-based mass spectrometry, enabling direct protein profiling of astrocytes in paraformaldehyde-fixed, optimal cutting temperature (OCT)-embedded mouse brain tissue. By applying this approach, we uncovered distinct region-associated astrocyte proteomic signatures in the cerebral cortex and hippocampus and selected novel candidate protein markers for subsequent validation by immunofluorescence. Notably, MINK1 and PLEKHB1 showed preferential expression in hippocampal and cortical astrocytes, respectively, highlighting their potential as region-specific astrocyte markers. Overall, this strategy enables high-precision, unbiased spatial proteomic discovery at subcellular resolution, providing a powerful framework for linking molecular diversity to functional specialization in astrocyte biology. - Source: PubMed
Publication date: 2026/07/17
Huang Chien-ChangChang Chiung-YunChan Po-ChaoChong Weng ManChang Hsiao-JenLiao Jung-Chi - A major challenge facing prostate cancer (PCa) cells is oxidative stress, yet the precise role and underlying mechanisms remain inadequately elucidated. The study sought to investigate the association between oxidative stress and PCa prognosis, as well as to identify potential regulatory pathways involved. - Source: PubMed
Publication date: 2026/07/08
Liang ShuaiZhou ShuhuaTang YangshuoXiao MoyanYe Ke - Chemotherapy-induced peripheral neuropathy (CIPN) is a major dose-limiting side effect of cancer treatment, yet the lack of predictive human models continues to hinder therapeutic progress. Here, we establish a scalable and reproducible model of paclitaxel-induced axon degeneration and neurotoxicity in human iPSC-derived sensory neurons, suitable for high-throughput identification of neuroprotective compounds. Using this platform, we screen a library of 192 kinase inhibitors and identify 19 hits that commonly inhibit three STE20 kinases-MAP4K4, MINK1, and TNIK. Genetic knockdown studies reveal that multi-kinase inhibition of these kinases is required for neuroprotection against paclitaxel. Consistently, selective pharmacological inhibition of the identified STE20 kinases rescues paclitaxel-induced axon degeneration in iPSC-derived sensory neurons and primary human dorsal root ganglia (DRG) and preserves intraepidermal nerve fiber density in a mouse model of CIPN. Together, these findings establish a translational human sensory neuron platform that enables target validation and drug discovery for CIPN. - Source: PubMed
Publication date: 2026/05/06
Petrova VeselinaMills Caitlin EHug ClemensCetinkaya-Fisgin AyselSplaine JenniferFouladzadeh SepidehHakim SaraPowell RasheenZhen ShannonChung MirraBradshaw Gary ADeng TaoSingec IlyasWang QingKawaguchi RikiJonnagaddala HarathiBarrett Lee BSmith Jennifer AKalocsay MarianGyori Benjamin MHoke AhmetSorger Peter KWoolf Clifford J - The nucleotide oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome is a cytosolic multiprotein complex that can be activated by a wide variety of stimuli. However, dysregulated activation of NLRP3 is implicated in the pathogenesis of chronic inflammatory diseases. Hence, the activity of NLRP3 is intricately governed by several regulatory mechanisms. Misshapen-like kinase 1 (MINK1), a serine/threonine kinase, plays an important role in the immune cell differentiation and inflammatory response regulation in mammals; however, its regulatory function in NLRP3 inflammasome activation in fish remains poorly understood. In the present study, a homolog gene of MINK1 (MINK1) was cloned and functionally characterized in common carp ( L.). The expression profiling disclosed that was upregulated under spring viremia of carp virus (SVCV) and stimulation. Overexpression of MINK1 promoted NLRP3-mediated inflammasome activation, including apoptosis-associated speck-like protein containing a CARD (ASC) oligomerization, speck formation, cysteine-requiring aspartate protease A/B (Caspase-A/B) enzyme activity and interleukin-1β (IL-1β) cleavage. Mechanistically, MINK1 interacted with NLRP3 via its S_TKC domain and facilitated NLRP3 phosphorylation, thereby promoting its aggregation and activation. Collectively, these discoveries unveil a novel regulatory mechanism that governs the functional regulation of NLRP3 and fine-tuning innate immune responses in teleost. - Source: PubMed
Publication date: 2025/10/22
Liu RongrongZhao KeyingZhao YueYang GuiwenLi Hua