MARK4 antibody
- Known as:
- MARK4 (anti-)
- Catalog number:
- orb101859
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- MARK4 antibody
Related genes to: MARK4 antibody
- Gene:
- MARK4 NIH gene
- Name:
- microtubule affinity regulating kinase 4
- Previous symbol:
- MARKL1
- Synonyms:
- Nbla00650, FLJ90097, KIAA1860, PAR-1D
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-25
- Date modifiied:
- 2016-02-10
Related products to: MARK4 antibody
Related articles to: MARK4 antibody
- Human neural organoids (NOs) provide a powerful platform for investigating synaptic development and dysfunction during early neurodevelopment. However, methodologies for isolating functional synaptic structures from these models remain limited. Here, we present a differential centrifugation protocol enabling the enrichment of growth cone particles (GCPs) and immature synaptosomes from air-liquid interface cerebral organoids (ALI-COs) at distinct developmental stages (Day 90 and 150). Notably, the method avoids density gradients, requires minimal starting material while maintaining reproducibility across human and murine tissues. Quantitative proteomic profiling revealed significant enrichment of growth cone markers (e.g., GAP43) and classical synaptosomal proteins (e.g., PCLO, BSN, SYN1). Transmission electron microscopy (TEM) confirmed the presence of membrane-enclosed GCPs with fibrous content and mitochondria in Day 90 isolates, and immature synaptosomes containing synaptic vesicles on day 150. Functional viability of both types of synaptic structures was demonstrated through KCl-induced depolarization, which triggered phosphorylation changes in growth cone proteins (GAP43, MARCKS, MARCKSL1), cytoskeletal regulators (DCLK1, SHTN1, MARK4, MAP1B) and protein kinases (CAMK2G, PRKCE) in Day 90 GCPs, as well as classical synaptic vesicle cycle proteins (SYN1, DNM1, RPH3A) at Day 150. Overall, this study establishes a centrifugation-based protocol for isolating growth cones and immature synapses from human organoids, capturing key stages of synaptic development and enabling scalable, patient-compatible models to study synaptic function and dysfunction in neurodevelopmental and neurodegenerative disorders. - Source: PubMed
Øhlenschlæger Marie SCriscuolo LucreziaJensen PiaLloyd-Davies Sánchez Daniel JSutcliffe MagdalenaBhosale SantoshBogetofte HelleTahir MuhammadJakobsen Lene APihl MariaBrewer JonathanSchwämmle VeitPoulsen Frantz RFreude KristineLancaster Madeline ARobinson Phillip JLarsen Martin R - Microglia dynamically remodel their cytoskeleton to surveil the brain, respond to injury, and shape synaptic connectivity. While actin drives rapid process motility and phagocytic cup formation, emerging evidence indicates that microtubules are critical regulators of microglial morphology, trafficking, and inflammatory signaling. In homeostatic microglia, microtubules are nucleated at Golgi outposts, supporting ramified architectures and low inflammatory tone. Upon activation, microglia undergo a switch to a centrosome-nucleated, radial microtubule array, driven in part by cyclin-dependent kinase 1 (Cdk1) and associated with polarized cytokine release, NLRP3 inflammasome engagement, and altered phagocytic behavior. We discuss how key regulators of this transition-including Cdk1, centrosomal γ-tubulin recruitment, Golgi-derived microtubule nucleation, and the kinase MARK4 may constitute druggable nodes to tune microglial reactivity in neuro-degenerative diseases. Finally, we outline experimental priorities for translating microglial microtubules into therapeutic targets. - Source: PubMed
Publication date: 2026/04/20
Sanchini CaterinaRosito MariaBartolini FrancescaDi Angelantonio Silvia - Triple-negative breast cancer (TNBC) is the most challenging breast cancer subtype to treat due to the absence of effective targeted therapies. In this study, we demonstrate that elevated expression of microtubule affinity-regulating kinase 2 (MARK2), but not other MARK family members (MARK1, MARK3, and MARK4), correlates with poor prognosis in TNBC patients. Silencing MARK2 impairs TNBC progression via inhibition of mutant p53 (mutp53) signaling. In contrast, silencing any of the other three MARKs either enhances or does not affect TNBC cell growth or migration and has no impact on mutp53 expression. Notably, direct knockdown of mutp53 recapitulates the effects of MARK2 ablation in TNBC cells, further supporting a functional linkage. Moreover, ectopic expression of either wild-type (WT) MARK2 or its kinase-dead (KD) mutant enhances mutp53 signaling and promotes TNBC progression; however, MARK2 overexpression does not alter wild-type p53 (wtp53) expression or cell growth in luminal breast cancer cells. Significant inverse correlations are also observed between the expression levels of MARK2, THBS1, or HBEGF (two direct target genes of mutp53) and both overall and disease-free survival in TNBC patients harboring mutTP53, whereas no such association exists between MARK2 and survival in breast cancer subtypes expressing wtTP53. MARK2 is predominantly localized in the nucleus of TNBC cells, where it interacts with and stabilizes mutp53 through its UBA and Spacer domains. Consistent with this, MARK2-ΔUBA or MARK2-ΔSpacer mutant proteins fail to bind mutp53 or sustain its signaling, thereby acting as dominant-negative inhibitors that suppress TNBC progression. Collectively, our findings indicate that suppressing MARK2 expression, rather than inhibiting its kinase activity, may represent an effective therapeutic strategy for TNBC with mutTP53. - Source: PubMed
Zhang MinZhu XilongCui MengqianGuan YinanZhang YongWeiss Stephen JChen JunYao YongzhongFu RongWu Zhaoqiu - Mitochondrial homeostasis is intimately associated with the toxic effects of exogenous chemicals, as well as the onset and progression of various diseases. Benzo[b]fluoranthene (BbF) is ubiquitously distributed across various environmental media. The association between BbF exposure and male reproductive damage has been recently discovered. However, the relevant mechanisms remain unexplored. - Source: PubMed
Publication date: 2026/03/17
Shi Chao-FengHan FeiJiang XiaoSun LeiLiu Kang-leSun Sheng-QiLi Ying-QingWang Jian-KangAo LinCao JiaChen QingLiu Jin-Yi - The incidence of diabetic cardiomyopathy (DCM) is increasing significantly as the population ages. DCM is one of the main causes of heart failure and mortality among patients with diabetes. Impaired mitophagy leads to mitochondrial dysfunction, which in turn aggravates DCM progression. Microtubule affinity-regulating kinase 4 (MARK4) is a key regulator of autophagy in adipocytes. - Source: PubMed
Wu YiWang Wei-YiZhang Jing-QiWang SaiZeng ZhiFu LuLi Bin