Ask about this productRelated genes to: RAB14 Blocking Peptide
- Gene:
- RAB14 NIH gene
- Name:
- RAB14, member RAS oncogene family
- Previous symbol:
- -
- Synonyms:
- FBP, RAB-14
- Chromosome:
- 9q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-14
- Date modifiied:
- 2015-02-02
Related products to: RAB14 Blocking Peptide
Related articles to: RAB14 Blocking Peptide
- Insulin attenuates the effects of advanced glycation end products (AGEs) by inducing a disintegrin and metalloprotease 10 (ADAM10)-mediated cleavage of the receptor for AGEs (RAGE); however, the molecular mechanism underlying this process remains incompletely understood. We investigated the mechanism by which insulin promotes ADAM10-mediated RAGE shedding in cultured human aortic endothelial cells (HAECs). AGE-modified bovine serum albumin (AGE-BSA) increased intercellular adhesion molecule-1 (ICAM-1) expression, whereas insulin pretreatment (0.1-100 nM) attenuated this effect. Mechanistically, insulin activated AKT1, AKT2, and AKT3, promoted ADAM10 translocation to the cell surface, and enhanced RAGE ectodomain shedding. In contrast, treatment with GI254023X (an ADAM10 inhibitor) or ADAM10 knockdown using siRNA abolished insulin-induced RAGE ectodomain shedding. Likewise, knockdown of AKT1, AKT2, or AKT3 using siRNA, as well as treatment with the pan-AKT inhibitor MK-2206, inhibited insulin-induced ADAM10 cell surface translocation and RAGE ectodomain shedding. Co-immunoprecipitation analysis further demonstrated an interaction between Rab14 and ADAM10. Insulin enhanced this interaction and promoted the translocation of both Rab14 and ADAM10 to the cell surface. Conversely, Rab14 knockdown blocked insulin-induced ADAM10 cell surface translocation and RAGE ectodomain shedding, thereby abolishing the protective effect of insulin against AGE-BSA-induced ICAM-1 expression. Collectively, these findings demonstrate that insulin promotes Rab14-mediated trafficking of ADAM10 to the cell surface through AKT activation in HAECs, resulting in enhanced RAGE ectodomain shedding. - Source: PubMed
Publication date: 2026/09/18
Baek Chung HeeKim HyosangMoon Soo YoungLee Eun KyoungYang Won Seok - Salmonella enterica serovar Typhimurium (S. Typhimurium) is a major cause of foodborne infections and represents a significant public health concern. After entering host cells, S. Typhimurium uses effector proteins to support its intracellular survival, but the mechanisms through which these effectors act remain incompletely understood. In this study, we investigated PipB2 as a Salmonella effector associated with increased intracellular bacterial survival and characterized Rab14 as a PipB2-associated host target. We found that recombinant PipB2 directly bound Rab14 and reduced Rab14 GTP hydrolysis in vitro, while the presence of PipB2 in infected cells was associated with increased phosphorylation of AKT and AS160, suggesting that PipB2 may affect Rab14-related host processes and may also be linked to AKT-AS160-associated host signaling. These PipB2-associated changes were accompanied by impaired autophagic flux and increased intracellular bacterial burden, consistent with enhanced intracellular replication. Pharmacological inhibition of AKT with inhibitor VIII partially attenuated PipB2-associated changes in autophagic flux and reduced intracellular bacterial burden both in vitro and in vivo. Our mechanistic investigations provide new insights into how the S. Typhimurium effector PipB2 impairs host autophagic flux and suggest a potential host-directed intervention strategy. - Source: PubMed
Publication date: 2026/08/07
Zhu TingDai ChangzhiLi JiayiPan PengShen RuiGou HongchaoSun DageChen KaifengChang YuxinXu ChenggangLiao MingZhang Jianmin - Glucocorticoid-induced osteoporosis (GIO) is driven by a pathogenic shift in bone marrow mesenchymal stem cell (BMSC) lineage commitment from osteogenesis to adipogenesis. Here, we identify Microtubule Actin Cross-linking Factor 1 (MACF1) as a critical regulator of MSC fate that is severely suppressed during long-term glucocorticoid (GC) exposure. We demonstrate that MACF1 deficiency phenocopies GC-induced marrow adiposity and bone loss. Crucially, restoring endogenous MACF1 via promoter-targeted small activating RNA (saRNA) effectively corrects this fate bias and reverses microarchitectural deterioration in GIO mice. Mechanistically, MACF1 acts as a key facilitator of vesicular trafficking. By orchestrating the assembly of the Rab14/KIF16B complex, MACF1 drives the precise anterograde transport of Fibroblast Growth Factor Receptors (FGFRs) to the plasma membrane. GC exposure downregulates MACF1, disrupting this transport machinery and causing intracellular FGFR sequestration. This transport failure depletes functional cell-surface FGFRs, thereby blunting osteogenic signaling and triggering the adipogenic shift. Collectively, our findings establish the MACF1-governed intracellular trafficking network as an important determinant of FGFR spatial distribution and MSC fate, highlighting it as a promising therapeutic target for restoring bone-fat equilibrium in GIO. - Source: PubMed
Publication date: 2026/08/10
Su PeihongTian YeZhao FanLi JingPatil SuryajiZhu ChunyuTian YujiaWang JunrongLiu JiatingXiang AoqiGuan HuaZhang LushaChen XiaochangQian AirongYu Qi - spp. are widespread intracellular animal pathogens that cause brucellosis, a significant zoonosis. Despite the global impact of brucellosis on animal and human health, the host genes that support infection remain incompletely defined. To address this knowledge gap, we developed a flow cytometry-based infection assay with fluorescent and performed a genome-wide CRISPR-Cas9 loss-of-function screen in human macrophage-like cells. Disruption of >150 host genes significantly reduced intracellular signal at 3 hours post-infection. In addition to recovering known host factors, the screen revealed previously unappreciated genes linked to endosomal trafficking, cytoskeletal remodeling, and lipid homeostasis. The screen was robust, as validation within these functional categories confirmed that the small GTPase RAB14, the Src-family kinase regulator CSK, and the phospholipid flippase subunit TMEM30A support the and infection process at a post-entry step. Gene set enrichment analysis further identified positive regulators of mTORC1 signaling as host factors. This result was validated by genetic disruption of LAMTOR2 and AKT1, and pharmacologic inhibition of AKT1. Together, these data indicate that the AKT-Ragulator-mTORC1 axis contributes to establishing a permissive intracellular niche. Finally, to assess whether these host requirements extend beyond , we examined infection by the unrelated intracellular pathogen . CSK, AKT1, and LAMTOR2 were required for efficient infection, whereas RAB14 was dispensable. Together, these results define host genes that impact infection and distinguish shared versus pathogen-specific host dependencies exploited by intracellular bacteria. - Source: PubMed
Publication date: 2026/06/30
Kim ThomasScheeres Eleanor CFiebig ArethaOlive Andrew JCrosson Sean - Antibody-dependent enhancement (ADE) is a major determinant of disease severity in flavivirus infections, yet the host-associated factors that regulate the transition from antibody-mediated uptake to productive infection remain incompletely defined. Fc gamma receptor IIA (FcγRIIA/CD32A), an activating Fc receptor expressed on myeloid cells, represents a key host determinant linking pre-existing immunity to viral entry pathways. Here, we investigated how FcγRIIA signalling influences intracellular trafficking and ADE efficiency across dengue virus (DENV), Zika virus (ZIKV), and Japanese encephalitis virus (JEV). - Source: PubMed
Publication date: 2026/06/17
Rakwi Nensar Wai Wai PhyoMuraoka DaisukeHaga KazumiYeo Adeline Syin LianMoi Meng Ling