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Recombinant Human CALCOCO1 Protein

  • 中文名: 重组人钙结合和卷曲螺旋结构域含蛋白1(CALCOCO1)
  • 别    名: CALCOCO1; KIAA1536; PP13275; UNQ2436/PRO4996Calcium-binding and coiled-coil domain-containing Protein 1; Calphoglin; Coiled-coil coactivator Protein; Sarcoma antigen NY-SAR-3
货号: PA2000-6422
Price: ¥询价
数量:
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产品详情

纯度>90%SDS-PAGE.
种属Human
靶点CALCOCO1
Uniprot NoQ9P1Z2
内毒素< 0.01EU/μg
表达宿主E.coli
表达区间1-691aa
氨基酸序列MEESPLSRAPSRGGVNFLNVARTYIPNTKVECHYTLPPGTMPSASDWIGIFKVEAACVRDYHTFVWSSVPESTTDGSPIHTSVQFQASYLPKPGAQLYQFRYVNRQGQVCGQSPPFQFREPRPMDELVTLEEADGGSDILLVVPKATVLQNQLDESQQERNDLMQLKLQLEGQVTELRSRVQELERALATARQEHTELMEQYKGISRSHGEITEERDILSRQQGDHVARILELEDDIQTISEKVLTKEVELDRLRDTVKALTREQEKLLGQLKEVQADKEQSEAELQVAQQENHHLNLDLKEAKSWQEEQSAQAQRLKDKVAQMKDTLGQAQQRVAELEPLKEQLRGAQELAASSQQKATLLGEELASAAAARDRTIAELHRSRLEVAEVNGRLAELGLHLKEEKCQWSKERAGLLQSVEAEKDKILKLSAEILRLEKAVQEERTQNQVFKTELAREKDSSLVQLSESKRELTELRSALRVLQKEKEQLQEEKQELLEYMRKLEARLEKVADEKWNEDATTEDEEAAVGLSCPAALTDSEDESPEDMRLPPYGLCERGDPGSSPAGPREASPLVVISQPAPISPHLSGPAEDSSSDSEAEDEKSVLMAAVQSGGEEANLLLPELGSAFYDMASGFTVGTLSETSTGGPATPTWKECPICKERFPAESDKDALEDHMDGHFFFSTQDPFTFE
分子量103.7 kDa 
蛋白标签GST-tag at N-terminal
缓冲液0
稳定性 & 储存条件Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt.
Reconstituted protein solution can be stored at 2-8°C for 2-7 days.
Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months.
复溶Always centrifuge tubes before opening.Do not mix by vortex or pipetting.
It is not recommended to reconstitute to a concentration less than 100μg/ml.
Dissolve the lyophilized protein in distilled water.
Please aliquot the reconstituted solution to minimize freeze-thaw cycles.


参考文献

以下是关于CALCOCO1的3篇关键参考文献及其简要概括:

1. **文献名称**:CALCOCO1 is a soluble autophagy receptor for a subset of client proteins

**作者**:Behrends C, et al. (2010)

**摘要**:研究发现CALCOCO1(也称为SQSTM1-interacting protein)通过与LC3和GABARAP蛋白互作,在选择性自噬过程中作为接头蛋白,负责识别并运输泛素化底物至自噬体,调控细胞稳态。

2. **文献名称**:CALCOCO1/TRIM23 inhibits type I interferon induction by targeting IRF3

**作者**:Inn KS, et al. (2011)

**摘要**:揭示CALCOCO1通过其卷曲螺旋结构域结合干扰素调节因子IRF3.抑制病毒触发的IRF3激活和下游干扰素信号通路,表明其在天然免疫应答中的负调控作用。

3. **文献名称**:Structural basis for recognition of autophagic receptor CALCOCO1/NDP52 by the TRIM21 ubiquitin ligase

**作者**:Ji CH, et al. (2021)

**摘要**:通过冷冻电镜解析CALCOCO1与TRIM21的复合物结构,揭示二者通过卷曲螺旋结构域相互作用,调控内质网应激诱导线粒体自噬的分子机制,为相关疾病治疗提供靶点依据。

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*注:若需更早或特定研究方向的文献,建议通过PubMed或Google Scholar以"CALCOCO1"+"autophagy"/"immune signaling"等关键词进一步检索。*


背景信息

CALCOCO1 (Calcium-Binding and Coiled-Coil Domain-Containing Protein 1), also known as Sperizin, is a multifunctional adaptor protein encoded by the CALCOCO1 gene in humans. Structurally, it contains an N-terminal calcium-binding domain, a central coiled-coil region, and a C-terminal motif that facilitates interactions with other proteins, such as ubiquitin or LC3-family members. These features enable CALCOCO1 to serve as a scaffolding molecule in diverse cellular processes.

Primarily studied for its role in selective autophagy, CALCOCO1 acts as a receptor that targets ubiquitinated substrates, including damaged mitochondria (mitophagy) and intracellular pathogens (xenophagy), to autophagosomes for degradation. It interacts with autophagy machinery via its LC3-interacting region (LIR), bridging cargo recognition to autophagosome formation. Beyond autophagy, CALCOCO1 modulates innate immune signaling by regulating NF-κB and type I interferon pathways, often through interactions with TRAF proteins or RIG-I-like receptors. It also participates in membrane trafficking and cell adhesion processes, impacting cancer metastasis and neuronal development.

CALCOCO1 dysregulation has been linked to diseases such as cancer, neurodegenerative disorders, and infections. For example, reduced expression correlates with poor prognosis in certain cancers, while its overexpression may mitigate neurotoxicity in Alzheimer's models. Despite these insights, its precise mechanisms and tissue-specific roles remain under investigation. Studies using knockout models highlight its non-redundant functions compared to homologs like CALCOCO2/NDP52. Further research may unveil therapeutic targets for autophagy-related pathologies.


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