人 NKIRAS1 抗体对
01AB02512
NFKB inhibitor interacting Ras like 1 (NKIRAS1), also known as kappaB-Ras1, is an atypical small GTPase that serves as a critical regulator of inflammatory and oncogenic signaling pathways. Unlike classical RAS proteins, NKIRAS1 lacks a C-terminal CAAX motif and exhibits reduced intrinsic GTP hydrolysis, allowing it to function in both GTP- and GDP-bound states. It primarily acts by binding to IkappaBbeta and the NF-kappaB RelA (p65) subunit, which stabilizes IkappaBbeta and prevents the phosphorylation events necessary for NF-kappaB activation. This mechanism effectively restrains TNF-alpha-induced transcription. Additionally, NKIRAS1 interacts with the RalGAP complex to enhance its activity, thereby negatively regulating Ral small GTPase signaling to control cell proliferation and metastasis. Clinically, NKIRAS1 is associated with Diamond-Blackfan anemia 12. Its frequent downregulation across various tumors suggests a tumor-suppressor role, as it simultaneously limits inflammation-driven and Ras/Ral-mediated oncogenesis.
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技术参数
- 靶点基因名
- NKIRAS1
- 基因别名
- KBRAS1
- 蛋白别名
- NFKB inhibitor interacting Ras like 1; NKIRAS1
- UniProt
- Q9NYS0
- 物种
- Human
产品详情
- 靶点名称
- NKIRAS1
- 蛋白名称
- NFKB inhibitor interacting Ras like 1
- 蛋白别名
- NF-kappa-B inhibitor-interacting Ras-like protein 1; I-kappa-B-interacting Ras-like protein 1; Kappa B-Ras protein 1; KappaB-Ras1
- 靶点基因名
- NKIRAS1
- 基因别名
- KBRAS1
- UniProt
- Q9NYS0
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
NFKB inhibitor interacting Ras like 1 (NKIRAS1), also known as kappaB-Ras1, is an atypical small GTPase that serves as a critical regulator of inflammatory and oncogenic signaling pathways. Unlike classical RAS proteins, NKIRAS1 lacks a C-terminal CAAX motif and exhibits reduced intrinsic GTP hydrolysis, allowing it to function in both GTP- and GDP-bound states. It primarily acts by binding to IkappaBbeta and the NF-kappaB RelA (p65) subunit, which stabilizes IkappaBbeta and prevents the phosphorylation events necessary for NF-kappaB activation. This mechanism effectively restrains TNF-alpha-induced transcription. Additionally, NKIRAS1 interacts with the RalGAP complex to enhance its activity, thereby negatively regulating Ral small GTPase signaling to control cell proliferation and metastasis. Clinically, NKIRAS1 is associated with Diamond-Blackfan anemia 12. Its frequent downregulation across various tumors suggests a tumor-suppressor role, as it simultaneously limits inflammation-driven and Ras/Ral-mediated oncogenesis.