NKAP Antibody
- Known as:
- NKAP Antibody
- Catalog number:
- XW-7766
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- NKAP Antibody
Related genes to: NKAP Antibody
- Gene:
- NKAP NIH gene
- Name:
- NFKB activating protein
- Previous symbol:
- -
- Synonyms:
- FLJ22626
- Chromosome:
- Xq24
- Locus Type:
- gene with protein product
- Date approved:
- 2007-08-16
- Date modifiied:
- 2014-11-19
Related products to: NKAP Antibody
Related articles to: NKAP Antibody
- Hackman-Di Donato syndrome (Online Mendelian Inheritance in Man no. 301,039), caused by mutations of the NKAP gene, located in Xq24, is a rare genetic disorder characterized by a Marfanoid phenotype, intellectual disability, and abnormalities of the musculoskeletal system. This condition has only been described in ten patients and two fetuses, who were identified owing to severe heart defects. All previously reported patients had mutations located in exons 8 and 9 of NKAP. - Source: PubMed
Publication date: 2026/03/31
Semyachkina Alla NNikolaeva Ekaterina AGritsevskaya Daria IuVoinova Victoria YuKuramagomedova Rabiat GBochenkov Sergei VGroznova Olga SParfenenko Mariia AKalashnikova Olga VIsupova Evgenia A - NKAP (NF-kappa-B-activating protein) is a ubiquitously expressed nuclear protein involved in multiple biological processes. Males with missense mutations have been reported to present with marfanoid features and behavioral and musculoskeletal abnormalities. We have previously reported that a disruptive mutation resulted in extremely skewed X chromosome inactivation (XCI), leading to phenotypic manifestation of hemophilia A (HA) in a HA carrier. In this study, with the aim of exploring the phenotypic manifestations of deleterious mutations in males, as well as their involvement in the mechanism of XCI regulation in females, we generated mutant mice using CRISPR/Cas9 technology. Gait analysis studies conducted in male mice hemizygous for mutant by the CatWalk XT system revealed significant alterations in gait parameters, consistent with hypotonia reported in human mutant patients. By breeding mutant mice with HA mice, we generated a double heterozygous mutant NKAP/HA mouse model, i.e., female mice carrying mutant with a WT copy on one X chromosome, and WT with a mutant copy on the other X chromosome. XCI pattern analysis using methylation-sensitive restriction enzymes demonstrated that mutant NKAP/HA females exhibited significant XCI skewing of the X chromosome bearing the mutant copy. Furthermore, these females exhibited significantly reduced F8 mRNA levels and FVIII (factor VIII) antigen levels, as demonstrated by quantitative RT-PCR and ELISA, respectively. Murine embryonic fibroblasts (MEFs) derived from a hemizygous mutant embryo exhibited markedly reduced proliferation rate and increased senescence compared to WT MEFs, suggesting that XCI skewing induced by mutant results from secondary selection against cells with an active X chromosome bearing the mutant copy. - Source: PubMed
Publication date: 2026/03/02
Avishai EinatDardik RimaRubinstein LindaBudnik IvanBen Gera YairTwitto-Greenberg RachelKenet GiliLivnat TamiLevy-Mendelovich Sarina - NF-κB activating protein (NKAP) plays important roles in various cancers, including breast cancer. However, its expression and prognosis value in breast cancer remains uncertain. Gene expression profiling interactive analysis, Human protein atlas database, and University of Alabama at Birmingham Cancer data analysis portal database were used to predict the expression and prognostic value of NKAP in breast cancer. Immunohistochemistry, quantitative real time polymerase chain reaction (qRT-PCR) and western blot were performed to detect NKAP expression. The effects of NKAP on cell proliferation, migration and drug sensitivity were investigated in MDA-MB-231 and SK-BR-3 cells. NKAP protein expression differed in breast cancer tissues and paraneoplastic tissues based on the cancer genome atlas data. The high NKAP expression was significantly correlated with a poor prognosis in breast cancer patients. The results of immunohistochemistry, western blot assay, and qRT-PCR proved that NKAP was highly expressed in breast cancer tissues compared with paraneoplastic tissues. In addition, qRT-PCR results showed that high expression of NKAP was significantly correlated with the larger tumor size and higher TNM stage. Moreover, knockdown of NKAP significantly inhibited the proliferation, migration, and enhanced drug sensitivity of MDA-MB-231 and SK-BR-3 cells. NKAP is highly expressed in breast cancer tissues, and its high expression is closely associated with poor prognosis. NKAP also promotes proliferation, migration, and inhibits drug sensitivity of breast cancer cells. - Source: PubMed
Li YonghaoShu ZhengSun ChenyuLowe ScottBentley RachelLi YaruKing BethanyChen ShuyaZhou QinZhang Mei - Although there is a decline in the overall incidence of chronic gastritis through antibiotic treatment, the public health burden remains significant because of low eradication rates. Herein, we explore the role of sphingosine-1-phosphate receptor-2 (S1P receptor) in mediating the development of chronic gastritis, as well as the effect of S1P receptor antagonists in attenuating its development. - Source: PubMed
Publication date: 2025/12/30
Li Ke-QinSun Zhi-MengShao Han-BingTan Ming-YongYang MingHe Cheng-WeiCheng Yu-YaoZhang Xi-NanJiang Lei-LeiWan Sheng-BiaoCui Shu-XiangQu Xian-Jun - Inorganic polyphosphate (polyP), a conserved phosphate polymer, modulates protein function across diverse biological systems, yet its human protein interactome remains poorly defined. While prior studies identified denaturation-resistant polyP modifications on lysine-rich sequences in yeast and bacteria, such targets in human proteins were previously unknown. Here, we performed a systematic screen of 57 lysine-rich human proteins, selected via mass spectrometry and bioinformatics, identifying 41 proteins that exhibit denaturation-resistant polyP modifications. This marks the first identification of lysine-rich motifs as polyP targets in human proteins. Through mutagenesis and binding assays, we establish these lysine-rich motifs, rather than traditional PASK domains, are critical for polyP binding, with consecutive lysine residues and intrinsic disorder as key determinants. Functional assays demonstrate that polyP binding inhibits phase separation of the transcriptional regulator NKAP, suppresses K-RAS GTPase activation, and reduces DDX55 helicase activity, revealing direct regulatory mechanisms. This work not only marks the first identification of denaturation-resistant polyP modifications in human proteins but also provides a comprehensive resource for investigating polyP's roles in human cellular homeostasis and disease. - Source: PubMed
Publication date: 2025/11/29
Yang ZhiyunJin JinLehotsky KirstenMartins IsabellaBelrose EthanNeville NolanJia Zongchao