Ask about this productRelated genes to: KIF3C Blocking Peptide
- Gene:
- KIF3C NIH gene
- Name:
- kinesin family member 3C
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-03
- Date modifiied:
- 2016-10-05
Related products to: KIF3C Blocking Peptide
Related articles to: KIF3C Blocking Peptide
- Previous research has shown that exercise can produce cognitive benefits through neuroplastic mechanisms in older adults with mild cognitive impairment (MCI). This study builds on prior research by identifying biomarkers of neurological-related proteins that mediate improvement in processing speed in different exercise environments, water-based and land-based, in older adults with MCI. - Source: PubMed
Publication date: 2025/09/18
Savettiere AdrianaLam JovianNguyen Mary Hong-HoangSchulte TilmanHirst RaynaFairchild Jennifer Kaci - The recycling of integrin endocytosed during focal adhesion (FA) disassembly is critical for cell migration and contributes to the polarized formation of new FAs toward the leading edge. How this occurs is unclear. Here, we sought to identify the kinesin motor protein(s) that is involved in recycling endocytosed integrin back to the plasma membrane. We show that the kinesin-2 heterodimer, KIF3AC, and the Rab11 adaptor protein Rab coupling protein (RCP) are required for FA reformation after the disassembly of FAs in mouse and human fibroblasts. In the absence of KIF3AC, integrin does not return to the cell surface after FA disassembly and is found in the Rab11 endocytic recycling compartment. Biochemical pulldowns revealed that KIF3C associated with β1 integrin in an RCP-dependent fashion, but only after FA disassembly. KIF3AC knockdown inhibited cell migration, trafficking of RCP toward the leading edge, and polarized formation of FAs at the leading edge. These results show that KIF3AC promotes cell migration by recycling integrin so that it generates new FAs in a polarized fashion. - Source: PubMed
Publication date: 2025/07/24
Rockenbach Johnny A ZNader Guilherme P FAntoku SusumuGundersen Gregg G - Evidence indicated that KIF3C, a member of the kinesin superfamily of motor proteins, exhibits significant upregulation across various cancer types. Consequently, its impact on cancer advancement, including cell proliferation, migration, and invasion, is evident. Nonetheless, the comprehension of KIF3C's expression and role in colorectal cancer (CRC) remains limited. - Source: PubMed
Publication date: 2025/03/12
Diallo Maladho TantaChen BangquanYao QingYan ZhangSun QiannanWang Daorong - The recycling of integrin endocytosed during focal adhesion (FA) disassembly is critical for cell migration and contributes to the polarized formation of new FAs toward the leading edge. How this occurs is unclear. Here, we sought to identify the kinesin motor protein(s) that is involved in recycling endocytosed integrin back to the plasma membrane. We show that the kinesin-2 heterodimer, KIF3AC and the Rab11 adaptor protein RCP are required for FA reformation after the disassembly of FAs in mouse and human fibroblasts. In the absence of KIF3AC, integrin does not return to the cell surface after FA disassembly and is found in the Rab11 endocytic recycling compartment. Biochemical pulldowns revealed that KIF3C associated with β1 integrin in an RCP dependent fashion, but only after FA disassembly. KIF3AC knockdown inhibited cell migration, trafficking of RCP toward the leading edge, and polarized formation of FAs at the leading edge. These results show that KIF3AC promotes cell migration by recycling integrin so that it generates new FAs in a polarized fashion. - Source: PubMed
Publication date: 2024/12/12
Rockenbach Johnny A ZNader Guilherme P FAntoku SusumuGundersen Gregg G - KIF3C serves as a motor protein that facilitates axonal transport in neuronal cells. It belongs to the kinesin superfamily and plays a crucial role in the development of various cancers. However, the role of KIF3C in gastric cancer (GC) the third-highest cause of cancer-related deaths remains unclear. To investigate the regulatory mechanisms and expression patterns of KIF3C in GC and their implications for GC progression, we conducted a series of in vitro and in vivo experiments. - Source: PubMed
Publication date: 2024/11/21
Diallo Maladho TantaChen BangquanYan ZhangSun QiannanLiu GuanghaoWang YongRen JunWang Daorong