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- YLKBIO
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- 2026年01月27日
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- 详细信息
- 文献和实验
- 技术资料
- 供应商：
优利科（上海）生命科学有限公司
- 库存：
100
- 靶点：
详询
- 级别：
科研
- 目录编号：
/
- 克隆性：
多克隆
- 抗原来源：
详见说明书
- 保质期：
1年
- 抗体英文名：
Anti-IKK gamma/IKBKG
- 抗体名：
IKK gamma/IKBKG抗体
- 标记物：
详询
- 宿主：
兔
- 适应物种：
/
- 免疫原：
见产品详情
- 亚型：
IgG
- 形态：
冻干或液体
- 应用范围：
见产品详情
- 保存条件：
-20℃
- 浓度：
1mg/ml
- 规格：
详询
| 英文名称 Anti-IKK gamma/IKBKG |
| 中文名称 KB抑制蛋白激酶γ抗体 |
| 别 名 IkB kinase associated protein 1; IkB kinase subunit gamma; Inhibitor of nuclear factor kappa B kinase subunit gamma; AMCBX1; FIP 3; FIP3; Fip3p; I kappa B kinase gamma; IkB kinase associated protein 1; IkB kinase gamma subunit; IkB kinase subunit gamma; IKBKG; IKKAP 1; IKKAP1; IKKG; Incontinentia pigmenti; Inhibitor of kappa light polypeptide gene enhancer in B cells kinase gamma; Inhibitor of kappa light polypeptide gene enhancer in B cells, kinase gamma; Inhibitor of nuclear factor kappa B kinase gamma subunit; Inhibitor of nuclear factor kappa B kinase subunit gamma; IP 1; IP 2; IP; IP1; IP2; IPD2; NEMO; NF kappa B essential modifier; NF kappa B essential modulator; NF kappaB essential modifier; NF kappaB essential modulator; NFkappaB essential modulator. |
| 浓 度 1mg/1ml |
| 规 格 0.2ml/200μg |
| 抗体来源 Rabbit |
| 克隆类型 polyclonal |
| 交叉反应 Human, Mouse, Rat, Dog, Pig, Horse, Rabbit |
| 产品类型 一抗 |
研究领域 肿瘤 免疫学 染色质和核信号 信号转导 转录调节因子  |
| 蛋白分子量 predicted molecular weight: 46kDa |
| 性 状 Lyophilized or Liquid |
| 免 疫 原 KLH conjugated synthetic peptide derived from human IKK gamma |
| 亚 型 IgG |
| 纯化方法 affinity purified by Protein A |
| 储 存 液 0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide |
| 产品应用 WB=1:100-500 ELISA=1:500-1000 IP=1:20-100 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 |
| （石蜡切片需做抗原修复） |
| not yet tested in other applications. |
| optimal dilutions/concentrations should be determined by the end user. |
| 保存条件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| Important Note This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| 产品介绍 Pro inflammatory cytokines activate the transcription factor NF kappa B by stimulating the activity of a protein kinase that phosphorylates Ikappa B, an inhibitor of NF kappa B, at sites that trigger its ubiquitination and degradation. A large, cytokine responsive Ikappa B kinase (IKK) complex has been purified and the genes encoding 2 of its subunits have been cloned. These subunits, IKK alpha and Ikk beta, are protein kinases whose function is needed for NF kappa B activation by pro inflammatory stimuli. IKK is composed of similar amounts of IKK alpha, Ikk beta, which are differentially processed forms of a third subunit, IKK gamma. IKK gamma interacts preferentially with IKK beta and is required for the activation of the IKK complex. |
| Function : Regulatory subunit of the IKK core complex which phosphorylates inhibitors of NF-kappa-B thus leading to the dissociation of the inhibitor/NF-kappa-B complex and ultimately the degradation of the inhibitor. Also considered to be a mediator for TAX activation of NF-kappa-B. Could be implicated in NF-kappa-B-mediated protection from cytokine toxicity (By similarity). Essential for viral activation of IRF3. |
| Subunit : Homodimer; disulfide-linked. Component of the I-kappa-B-kinase (IKK) core complex consisting of CHUK, IKBKB and IKBKG; probably four alpha/CHUK-beta/IKBKB dimers are associated with four gamma/IKBKG subunits. The IKK core complex seems to associate with regulatory or adapter proteins to form a IKK-signalosome holo-complex. The IKK complex associates with TERF2IP/RAP1, leading to promote IKK-mediated phosphorylation of RELA/p65. Part of a complex composed of NCOA2, NCOA3, CHUK/IKKA, IKBKB, IKBKG and CREBBP. Interacts with COPS3, CYLD, NALP2, TRPC4AP and LRDD. Interacts with ATM; the complex is exported from the nucleus. Interacts with TRAF6. Interacts with HTLV-1 Tax oncoprotein; the interaction activates IKBKG. Interacts with TANK; the interaction is enhanced by IKBKE and TBK1. Part of a ternary complex consisting of TANK, IKBKB and IKBKG. Interacts with ZFAND5. Interacts with RIPK2. Interacts with TNIP1 and TNFAIP3; TNIP1 facilitates the TNFAIP3-mediated de-ubiquitination of IKBKG (By similarity). Interacts with TNFAIP3; the interaction is induced by TNF stimulation and by polyubiquitin. Binds polyubiquitin; the interaction is mediated by two domains; reports about the binding to 'Lys-63'-linked and/or linear polyubiquitin, respective binding affinities and stoichiometry are conflicting. Interacts with Shigella flexneri ipah9.8; the interaction promotes TNIP1-dependent 'Lys-27'-linked polyubiquitination of IKBKG which perturbs NF-kappa-B activation during bacterial infection. Interacts with NLRP10. |
| Subcellular Location : Cytoplasm. Nucleus. Note=Sumoylated NEMO accumulates in the nucleus in response to genotoxic stress. |
Tissue Specificity : Heart, brain, placenta, lung, liver, skeletal muscle, kidney and pancreas. |
| Post-translational modifications : Phosphorylation at Ser-68 attenuates aminoterminal homodimerization. |
| Polyubiquitinated on Lys-285 through 'Lys-63'; the ubiquitination is mediated by NOD2 and RIPK2 and probably plays a role in signaling by facilitating interactions with ubiquitin domain-containing proteins and activates the NF-kappa-B pathway. Polyubiquitinated on Lys-399 through 'Lys-63'; the ubiquitination is mediated by BCL10, MALT1 and TRAF6 and probably plays a role in signaling by facilitating interactions with ubiquitin domain-containing proteins and activates the NF-kappa-B pathway. Monoubiquitinated on Lys-277 and Lys-309; promotes nuclear export. Polyubiquitinated through 'Lys-27' by TRIM23; involved in antiviral innate and inflammatory responses. Linear polyubiquitinated on Lys-111, Lys-143, Lys-226, Lys-246, Lys-264, Lys-277, Lys-285, Lys-292, Lys-302, Lys-309 and Lys-326; the head-to-tail polyubiquitination is mediated by the LUBAC complex and plays a key role in NF-kappa-B activation. Polyubiquitinated on Lys-309 and Lys-321 via 'Lys-27'-linked ubiquitin by Shigella flexneri E3 ubiquitin-protein ligase ipah9.8, leading to its degradation by the proteasome. |
| Sumoylated on Lys-277 and Lys-309 with SUMO1; the modification results in phosphorylation of Ser-85 by ATM leading to a replacement of the sumoylation by mono-ubiquitination on these residues. |
| Neddylated by TRIM40, resulting in stabilization of NFKBIA and down-regulation of NF-kappa-B activity. |
| DISEASE : Defects in IKBKG are the cause of ectodermal dysplasia anhidrotic with immunodeficiency X-linked (EDAID) [MIM:300291]; also known as hypohidrotic ectodermal dysplasia with immunodeficiency (HED-ID). Is a form of ectoderma dysplasia, a heterogeneous group of disorders due to abnormal development of two or more ectodermal structures. Characterized by absence of sweat glands, sparse scalp hair, rare conical teeth and immunological abnormalities resulting in severe infectious diseases. |
| Defects in IKBKG are the cause of ectodermal dysplasia anhidrotic with immunodeficiency-osteopetrosis-lymphedema (OLEDAID) [MIM:300301]. |
| Defects in IKBKG are a cause of immunodeficiency NEMO-related without anhidrotic ectodermal dysplasia (NEMOID) [MIM:300584]; also called immunodeficiency without anhidrotic ectodermal dysplasia, isolated immunodeficiency or pure immunodeficiency. Patients manifest immunodeficiency not associated with other abnormalities, and resulting in increased infection susceptibility. Patients suffer from multiple episodes of infectious diseases. |
| Defects in IKBKG are the cause of susceptibility to X-linked familial atypical micobacteriosis type 1 (AMCBX1) [MIM:300636]; also known as X-linked disseminated atypical mycobacterial infection type 1 or X-linked susceptibility to mycobacterial disease type 1. AMCBX1 is the X-linked recessive form of Mendelian susceptibility to mycobacterial disease (MSMD). MSMD is a congenital syndrome resulting in predisposition to clinical disease caused by weakly virulent mycobacterial species, such as bacillus Calmette-Guerin vaccines and non-tuberculous, environmental mycobacteria. Patients are also susceptible to the more virulent species Mycobacterium tuberculosis. |
| Defects in IKBKG are the cause of recurrent isolated invasive pneumococcal disease type 2 (IPD2) [MIM:300640]. Recurrent invasive pneumococcal disease (IPD) is defined as two episodes of IPD occurring at least 1 month apart, whether caused by the same or different serotypes or strains. Recurrent IPD occurs in at least 2% of patients in most series, making IPD the most important known risk factor for subsequent IPD. |
| Defects in IKBKG are the cause of incontinentia pigmenti (IP) [MIM:308300]; formerly designed familial incontinentia pigmenti type II (IP2). IP is a genodermatosis usually prenatally lethal in males. In affected females, it causes abnormalities of the skin, hair, eyes, nails, teeth, skeleton, heart, and central nervous system. The prominent skin signs occur in four classic cutaneous stages: perinatal inflammatory vesicles, verrucous patches, a distinctive pattern of hyperpigmentation and dermal scarring. |
| Similarity : Contains 1 C2HC-type zinc finger. |
| Database links : UniProtKB/Swiss-Prot: Q9Y6K9.2 human |
UniProtKB/Swiss-Prot: O88522.2mouse |
| MMP-14(Matrix metalloproteinase-14) 金属基质蛋白酶-14 |
| GFRα-1（GDNF family receptor alpha-1） GDNF家族受体α-1（抗原） |
| GLUT2(Glucose transporter type 2） 葡萄糖转运蛋白2（抗原） |
| GFRA4 ( Persephin receptor ) (GFR receptor alpha 4) GDNF家族受体α-4（抗原） |
| GHRF (GHRH) 生长激素释放激素（因子）（抗原） |
| ANGPTL1/ANG-1 (Angiopoietin-like Protein 1) 血管位蛋白样1/血管生成素样蛋白-1抗原 |
| GLUT4(Glucose transporter type 4） 葡萄糖转运蛋白4（抗原） |
| GIP （Gastric Inhibitory polypeptide） 胃泌素抑制肽（抗原） |
| GLP-2（Glucagon-like peptide-2） 胰高血糖素样肽-2（多肽抗原） |
| GRP94 （gp96） 94kDa 糖调节蛋白（抗原） |
| G Protein(Guanine nucleotide-binding regulatory protein) G蛋白（鸟苷酸结合蛋白）（抗原） |
| GR (Glucocorticoid receptor) 糖皮质激素受体 多肽 |
| GSK-3β(NT) (Glycogen Synthase Kinase-3β) 糖原合酶激酶-3β（抗原） |
| CKR-L2（ G protein-coupled receptor-2 ） G蛋白偶联受体-2(抗原) |
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文献和实验相关实验
于JNK，而影响细胞的凋亡。 请各位高手指点一下 您所讲的问题即为在氧化应激的过程中JNK通路的“cross-talk”问题。目前研究的比较多的是有关氧化应激的过程中NF-kb通路通过其靶基因XIAP 和 GADD45对JNK起抑制效应（如图）。此外，还有研究指出，在氧化应激引起的凋亡过程中，MAPKs通路本身的一些激酶（如MKP1，3，5，7）也对JNK起抑制作用。 我知道的很有限，欢迎其他战友补充。
位点的序列，包括肽库和肽芯片 [5，6] 的多种技术可用来鉴定激酶底物。此外，一种 λ 噬菌体 cDNA 表达文库的固相磷酸化筛选 [ 7，8 」以及不同蛋白质相互作用筛选方法，如覆盖方法 [ 9，11] 和酵母双杂交系统 [ 12，14] 已被应用在这方面。最近，蛋白激酶被改造成可接受人工合成的腺苷三磷酸盐（环戊基 ATP ) 模拟物，并用于鉴定特异底物。初步的研究已经证明，通过激酶来研究磷酸化的蛋白质芯片是可行的 [ 18，19] 。为了确定磷酸化位点，抗磷酸化蛋白表位 [6] 的抗体将用于蛋白
因子FKHRLI能促进凋亡基因Fas―l和Bim等转录，Akt被激活后从细胞膜转移到细胞核并磷酸化FKHRLl。磷酸化的FKHRLl被转运出细胞核后与胞质蛋白14―3―3螯合在一起而失去了对靶基因的转录功能。此外，Akt也能正调节两种转录因子NF―κB和Bcl―2。NF―kB与许多细胞因子和生长因子引起的细胞分化、凋亡和生存有关。在正常状态下，NF―κB在胞质中与它的抑制因子I―κB结合在一起，失去转录活性。Akt能通过磷酸化激活IKK。(1―κB的激酶)，导致I―κB磷酸化、降解，并与NF―κB分离，被释放
KB抑制蛋白激酶γ抗体
￥1680
