ARPC4
- Known as:
- ARPC4
- Catalog number:
- Y214040
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ARPC4
Related genes to: ARPC4
- Gene:
- ARPC4 NIH gene
- Name:
- actin related protein 2/3 complex subunit 4
- Previous symbol:
- -
- Synonyms:
- p20-Arc, ARC20
- Chromosome:
- 3p25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-06
- Date modifiied:
- 2016-10-05
Related products to: ARPC4
Related articles to: ARPC4
- N-WASP and WASP can induce actin polymerization via Arp2/3 and were reported to be crucial for homology-directed repair (HDR) of DNA double-strand breaks (DSB). The underlying mechanism was suggested to involve nuclear actin polymerization, but the mechanistic details were debated. Unexpectedly, we show now that neither WASP nor N-WASP is required for HDR during CRISPR-mediated genome editing. Using knock-out and overexpression of N-WASP and WASP in U2OS cells, we did not detect alterations in total gene editing, HDR, or the ratio of HDR to non-homologous end joining (NHEJ) as assessed by different methods. Furthermore, we could not observe colocalization of HA-tagged WASP or N-WASP with DSBs. Finally, while the Arp2/3 inhibitor CK-666 and ARPC4 knockdown by siRNA reduced HDR efficiency in U2OS cells, this corresponded with a decreased transfection efficiency and a reduction of the HDR-proficient cell cycle phases S and G2/M. In summary, contrary to expectations, these data do not support a crucial role for N-WASP and WASP in DSB repair. - Source: PubMed
Publication date: 2026/04/10
Le Phan Thu HanBuchard AndersBrakebusch Cord - Intellectual disability with mild dysmorphic features may be attributed to perinatal complications such as neonatal hypoxia. However, chromosomal abnormalities may underlie these phenotypes. We report a case with rare copy number variants that are likely to have neurodevelopmental relevance. - Source: PubMed
Publication date: 2026/02/19
Rangel-Méndez Jorge ARubi-Castellanos RodrigoContreras-Capetillo SilvinaGonzález-Herrera LizbethPinto-Escalante Doris - Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest malignancies, due to its aggressive invasiveness and resistance to therapy. The dense, stiff extracellular matrix, composed primarily of collagen I and basement membrane components such as collagen IV and laminin, acts as a mechanical barrier that constrains PDAC invasion. We investigated whether the actin-related protein (Arp) 2/3 complex, a key actin nucleator, is essential for PDAC cells to overcome extracellular matrix stiffness and facilitate migration. CRISPR/Cas9 knockout of the Arpc4 gene in murine PDAC cell lines derived from Kras-driven transgenic mice resulted in substantially downregulated all Arp2/3 complex members. Inactivation of Arp2/3 significantly impaired PDAC cell migration, disrupted branched tubular structure formation in collagen I, and inhibited invasive front formation in organoid culture together with tumor-associated macrophages and fibroblasts. Mechanistically, β1 integrin signaling emerged as a key regulator of Arp2/3-dependent migration through collagen-rich matrices. Clinically, elevated expression of Arp2/3 complex components correlates with poor patient survival and basal-like differentiation subtypes, underscoring its role in disease progression. This study identifies the Arp2/3 complex and β1 integrin signaling as critical mediators of PDAC invasiveness and suggests them as potential therapeutic targets for mitigating PDAC progression. - Source: PubMed
Publication date: 2026/03/07
Yang XiufenQiao YinaSun YifengAbdelaal TamerSchuck KathleenAbdelrasoul HendDe La Torre CarolinaHermes MalteDong YanHu JingxiongFang ChaoHuang XiaoyanKahlert ChristophHerr IngridMichalski Christoph WKong Bo - invasion of host respiratory epithelial cells is a critical mechanism driving acute exacerbations of chronic obstructive pulmonary disease (AECOPD). Although previous studies have extensively demonstrated that dynamic changes in the actin cytoskeleton are central to the invasion of host cells by , the detailed mechanisms underlying the specific upstream signaling pathways and key regulators driving this process remain incompletely understood. Our study identifies and validates the essential roles of key Rho GTPase regulators (CDC42, Rac1, ArpC2, ArpC4) in actin polymerization during infection, thereby elucidating a more comprehensive and specific molecular mechanism. Invasion assays and Transmission electron microscopy (TEM) showed that the Rho GTPase signaling pathway modulates bacterial load in A549 cells by regulating macropinosome volume. Further experiments used strains 73-OR and ATCC 25238 to invade wild-type A549 cells, CDC42 A549 cells, Rac1 A549 cells, ArpC2 A549 cells and ArpC4A549 cells respectively. Invasion assays and TEM were performed to quantify internalized bacteria, macropinosome volume changes, and bacterial distribution; Western blot analyses and cellular immunofluorescence were used to measure F-actin/G-actin ratios and microfilament fluorescence intensity. These results indicate that Rho GTPase signaling pathway modulates invasion by regulating actin polymerization dynamics. Specifically, CDC42 and Rac1 are essential for actin polymerization and bacterial internalization. ArpC4 contributes to actin remodeling without influencing invasion, while ArpC2 is uninvolved in both processes. These findings provide a theoretical basis for targeting innate immunity to prevent and treat -induced AECOPD. - Source: PubMed
Publication date: 2026/02/17
Ma RuiruiCheng GuixueWu YunChen JiaweiLu RongqiLiu Yali - Microglial dynamics and homeostasis are crucial for maintaining central nervous system (CNS) function. To fulfill their homeostatic functions, microglia develop into ramified cells with highly dynamic cell protrusions. However, the detailed mechanisms underlying this developmental transition are largely unknown. Here, we investigate the role of the Actin-related protein 2/3 (Arp2/3) complex, a critical actin nucleator that controls the formation of actin branches, for the biology of tissue-resident microglia. By conditionally targeting Arpc4 in mice, we show that Arp2/3 depletion in tissue-resident microglia causes phenotypes beyond previously reported functions in other immune cell types. Our results identify an important role of Arp2/3 for controlling the developmental transition of microglia into cells with ramified morphology, homeostatic gene profile, and surveillance function in the CNS. Together, our results link actin remodeling to microglial maturation and activation, highlighting the Arp2/3 complex as a critical factor for maintaining the plasticity and preventing pathological activation of endogenous microglia. - Source: PubMed
Publication date: 2026/02/27
Safaiyan ShimaFrosch MaximilianBickel TomMonaco GianniDvir RoieMadry ChristianBosch Lance Fredrick PahutanKierdorf KatrinInnocenti MetelloPriller JosefPrinz MarcoLämmermann Tim