p70 S6 Kinase Antibody | Affinity Biosciences LTD|亲科生物官网

产品:	p70 S6 Kinase 抗体
货号:	AF6226
描述:	Rabbit polyclonal antibody to p70 S6 Kinase
应用:	WB IHC IF/ICC
文献验证:	WB
反应:	Human, Mouse, Rat
预测:	Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
分子量:	70kDa; 59kD(Calculated).
蛋白号:	P23443
RRID:	AB_2835100

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阻断肽(封闭肽)是特异性结合目标抗体和阻断抗体结合的多肽。这些多肽包含抗体识别的抗原表位。与阻断肽结合的抗体不再与靶蛋白上的表位结合。例如，在免疫印迹(WB)和免疫组化(IHC)中，通过比较被阻断抗体和未阻断抗体的染色，可以看到哪种染色是特异性的。

规格	价格	库存
50ul	RMB¥ 1250	现货
100ul	RMB¥ 2300	现货
200ul	RMB¥ 3000	现货

货期: 当天发货

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实验方案

产品描述

来源:

Rabbit

应用:

WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:

Human, Mouse, Rat

预测:

Bovine(100%), Horse(%), Sheep(%), Rabbit(%), Dog(%), Chicken(%), Xenopus(%)

克隆:

Polyclonal

特异性:

p70 S6 Kinase Antibody detects endogenous levels of total p70 S6 Kinase.

RRID:

AB_2835100
引用格式: Affinity Biosciences Cat# AF6226, RRID:AB_2835100.

偶联:

Unconjugated. 130

纯化:

The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).

保存:

Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.

别名:

展开/折叠

70 kDa ribosomal protein S6 kinase 1; KS6B1_HUMAN; p70 alpha; P70 beta 1; p70 ribosomal S6 kinase alpha; p70 ribosomal S6 kinase beta 1; p70 S6 kinase alpha; P70 S6 Kinase; p70 S6 kinase, alpha 1; p70 S6 kinase, alpha 2; p70 S6K; p70 S6K-alpha; p70 S6KA; p70(S6K) alpha; p70(S6K)-alpha; p70-alpha; p70-S6K 1; p70-S6K; P70S6K; P70S6K1; p70S6Kb; PS6K; Ribosomal protein S6 kinase 70kDa polypeptide 1; Ribosomal protein S6 kinase beta 1; Ribosomal protein S6 kinase beta-1; Ribosomal protein S6 kinase I; RPS6KB1; S6K; S6K-beta-1; S6K1; Serine/threonine kinase 14 alpha; Serine/threonine-protein kinase 14A; STK14A;

抗原和靶标

免疫原:

Uniprot:

P23443(KS6B1_HUMAN) >>Visit HPA database.

基因/基因ID:

RPS6KB1(6198)

表达:

P23443 KS6B1_HUMAN:

Widely expressed.

描述:

This gene encodes a member of the RSK (ribosomal S6 kinase) family of serine/threonine kinases. This kinase contains 2 non-identical kinase catalytic domains and phosphorylates several residues of the S6 ribosomal protein.

序列:

P23443 KS6B1_HUMAN:
Protein BLAST With
NCBI/
ExPASy/
Uniprot

MRRRRRRDGFYPAPDFRDREAEDMAGVFDIDLDQPEDAGSEDELEEGGQLNESMDHGGVGPYELGMEHCEKFEISETSVNRGPEKIRPECFELLRVLGKGGYGKVFQVRKVTGANTGKIFAMKVLKKAMIVRNAKDTAHTKAERNILEEVKHPFIVDLIYAFQTGGKLYLILEYLSGGELFMQLEREGIFMEDTACFYLAEISMALGHLHQKGIIYRDLKPENIMLNHQGHVKLTDFGLCKESIHDGTVTHTFCGTIEYMAPEILMRSGHNRAVDWWSLGALMYDMLTGAPPFTGENRKKTIDKILKCKLNLPPYLTQEARDLLKKLLKRNAASRLGAGPGDAGEVQAHPFFRHINWEELLARKVEPPFKPLLQSEEDVSQFDSKFTRQTPVDSPDDSTLSESANQVFLGFTYVAPSVLESVKEKFSFEPKIRSPRRFIGSPRTPVSPVKFSPGDFWGRGASASTANPQTPVEYPMETSGIEQMDVTMSGEASAPLPIRQPNSGPYKKQAFPMISKRPEHLRMNL

种属预测

种属预测:

score>80的预测可信度较高，可尝试用于WB检测。*预测模型主要基于免疫原序列比对，结果仅作参考，不作为质保凭据。

Species

Results

Score

Horse

100

Bovine

100

Sheep

100

Dog

100

Xenopus

100

Chicken

100

Rabbit

100

Pig

Zebrafish

Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

研究背景

P23443_KS6B1_HUMAN

功能:

Serine/threonine-protein kinase that acts downstream of mTOR signaling in response to growth factors and nutrients to promote cell proliferation, cell growth and cell cycle progression. Regulates protein synthesis through phosphorylation of EIF4B, RPS6 and EEF2K, and contributes to cell survival by repressing the pro-apoptotic function of BAD. Under conditions of nutrient depletion, the inactive form associates with the EIF3 translation initiation complex. Upon mitogenic stimulation, phosphorylation by the mammalian target of rapamycin complex 1 (mTORC1) leads to dissociation from the EIF3 complex and activation. The active form then phosphorylates and activates several substrates in the pre-initiation complex, including the EIF2B complex and the cap-binding complex component EIF4B. Also controls translation initiation by phosphorylating a negative regulator of EIF4A, PDCD4, targeting it for ubiquitination and subsequent proteolysis. Promotes initiation of the pioneer round of protein synthesis by phosphorylating POLDIP3/SKAR. In response to IGF1, activates translation elongation by phosphorylating EEF2 kinase (EEF2K), which leads to its inhibition and thus activation of EEF2. Also plays a role in feedback regulation of mTORC2 by mTORC1 by phosphorylating RICTOR, resulting in the inhibition of mTORC2 and AKT1 signaling. Mediates cell survival by phosphorylating the pro-apoptotic protein BAD and suppressing its pro-apoptotic function. Phosphorylates mitochondrial URI1 leading to dissociation of a URI1-PPP1CC complex. The free mitochondrial PPP1CC can then dephosphorylate RPS6KB1 at Thr-412, which is proposed to be a negative feedback mechanism for the RPS6KB1 anti-apoptotic function. Mediates TNF-alpha-induced insulin resistance by phosphorylating IRS1 at multiple serine residues, resulting in accelerated degradation of IRS1. In cells lacking functional TSC1-2 complex, constitutively phosphorylates and inhibits GSK3B. May be involved in cytoskeletal rearrangement through binding to neurabin. Phosphorylates and activates the pyrimidine biosynthesis enzyme CAD, downstream of MTOR. Following activation by mTORC1, phosphorylates EPRS and thereby plays a key role in fatty acid uptake by adipocytes and also most probably in interferon-gamma-induced translation inhibition.

翻译修饰:

Phosphorylation at Thr-412 is regulated by mTORC1. The phosphorylation at this site is maintained by an agonist-dependent autophosphorylation mechanism (By similarity). Activated by phosphorylation at Thr-252 by PDPK1. Dephosphorylation by PPP1CC at Thr-412 in mitochondrion.

细胞定位:

Cell junction>Synapse>Synaptosome. Mitochondrion outer membrane. Mitochondrion.
Note: Colocalizes with URI1 at mitochondrion.

Nucleus. Cytoplasm.

Cytoplasm.

组织特异性:

Widely expressed.

亚基结构:

Interacts with PPP1R9A/neurabin-1 (By similarity). Interacts with RPTOR. Interacts with IRS1. Interacts with EIF3B and EIF3C. Interacts with TRAF4. Interacts with POLDIP3. Interacts (via N-terminus) with IER5.

蛋白家族:

The autoinhibitory domain is believed to block phosphorylation within the AGC-kinase C-terminal domain and the activation loop.

The TOS (TOR signaling) motif is essential for activation by mTORC1.

Belongs to the protein kinase superfamily. AGC Ser/Thr protein kinase family. S6 kinase subfamily.

研究领域

· Cellular Processes > Transport and catabolism > Autophagy - animal. (View pathway)

· Environmental Information Processing > Signal transduction > ErbB signaling pathway. (View pathway)

· Environmental Information Processing > Signal transduction > HIF-1 signaling pathway. (View pathway)

· Environmental Information Processing > Signal transduction > mTOR signaling pathway. (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway. (View pathway)

· Environmental Information Processing > Signal transduction > AMPK signaling pathway. (View pathway)

· Environmental Information Processing > Signal transduction > TGF-beta signaling pathway. (View pathway)

· Environmental Information Processing > Signal transduction > Apelin signaling pathway. (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > EGFR tyrosine kinase inhibitor resistance.

· Human Diseases > Drug resistance: Antineoplastic > Endocrine resistance.

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer. (View pathway)

· Human Diseases > Cancers: Overview > Proteoglycans in cancer.

· Human Diseases > Cancers: Specific types > Colorectal cancer. (View pathway)

· Human Diseases > Cancers: Specific types > Pancreatic cancer. (View pathway)

· Human Diseases > Cancers: Specific types > Acute myeloid leukemia. (View pathway)

· Human Diseases > Cancers: Specific types > Breast cancer. (View pathway)

· Human Diseases > Cancers: Specific types > Hepatocellular carcinoma. (View pathway)

· Human Diseases > Cancers: Specific types > Gastric cancer. (View pathway)

· Human Diseases > Cancers: Overview > Choline metabolism in cancer. (View pathway)

· Organismal Systems > Aging > Longevity regulating pathway. (View pathway)

· Organismal Systems > Aging > Longevity regulating pathway - multiple species. (View pathway)

· Organismal Systems > Immune system > Fc gamma R-mediated phagocytosis. (View pathway)

· Organismal Systems > Endocrine system > Insulin signaling pathway. (View pathway)

文献引用

1). A rationally designed CD19 monoclonal antibody-triptolide conjugate for the treatment of systemic lupus erythematosus. Acta pharmaceutica Sinica. B, 2024 (PubMed: 39525579) [IF=14.7]

2). Activation of integrated stress response and disordered iron homeostasis upon combined exposure to cadmium and PCB77. JOURNAL OF HAZARDOUS MATERIALS, 2020 (PubMed: 31837937) [IF=12.2]

Application: WB Species: Human Sample: HEL cells

Fig. 5. Disordered iron homeostasis and inhibited mTORC1 activity upon exposure to CdCl2 and PCB77 at low dose. (A) The relative fluorescence intensity of CAeAM for measuring LIP to reflect intracellular iron availability (n = 3–4), and (B) Representative blots of FTH1 protein content to reflect iron storage. Analyses were performed after single or combined exposure to CdCl2 and PCB77 at 1 μM for 48 h. (C) Phosphorylated S6 and total S6 content to reflect mTORC1 activity as measured by Western blot. Ratio of FTH1 to eIF2αP and ratio of pS6 to S6 in the control group were defined as 1. Analyses were performed after single or combined exposure to CdCl2 and PCB77 at 1 μM for 48 h. a- significantly different from the control group. Data were presented in mean ± SE. P < 0.05 was considered statistically significant.

3). NCAPD2 inhibits autophagy by regulating Ca2+/CAMKK2/AMPK/mTORC1 pathway and PARP-1/SIRT1 axis to promote colorectal cancer. CANCER LETTERS, 2021 (PubMed: 34229059) [IF=9.1]

Application: WB Species: Human Sample: CRC cells

Fig. 2. NCAPD2 inhibited cell autophagy and disrupted autophagic flux via Ca2+/CAMKK2/AMPK/mTORC1 pathway. (A) Western blot analyses for phosphorylated mTOR (p-mTOR, S2448), phosphorylated p70S6K (p-p70S6K, T389/412), phosphorylated 4E-BP1 (p-4E-BP1, T70) and phosphorylated AKT (p-AKT, S473) in CRCC cells with different treatments as indicated. (B) Western blot of indicated proteins in cells treated with mTORC1 inhibitor Rapamycin (3 nM, 24h). (C) Immunofluorescence staining of LC3II (red) and P62 (red) in CRC cells with different treatments as indicated. Merged images represented overlays of LC3II or P62 and nuclear staining by DAPI (blue). (D) Intracellular Ca2+ levels were analyzed by flow cytometry after staining with the fluorescent probe Fluo-3, AM in CRC cells. (E) Representative Western blot gel documents of phosphorylated CAMKK2(S511), phosphorylated AMPK(T172), phosphorylated mTOR(S2448), Beclin, ATG5, P62, LC3II in CRC cells with different treatments. (F) Western blots of indicated proteins in cells treated with an inhibitor of microsomal Ca2+-ATPase Thapsigargin (1 μM, 6h) and Ca2+ chelator BAPTA-AM (10 μM, 12h) respectively. Results are shown as mean ± s.d, *P < 0.05, **P < 0.01, ***P < 0.001, based on Student’s t-test. . (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

4). Inhibition of PTP1B blocks pancreatic cancer progression by targeting the PKM2/AMPK/mTOC1 pathway. Cell Death & Disease, 2019 (PubMed: 31745071) [IF=8.1]

Application: WB Species: Human Sample: pancreatic cancer tissue

Fig. 6 The relationship between PTP1B and AMPK. a PTP1B overexpression resulted in decreased p-AMPK (alpha). b, c The negative correlation between PTP1B and p-AMPKα was showed in pancreatic cancer patient tissue samples (p < 0.001, p value was obtained by a Pearson χ2 test; scale bar, 200 μm and 50 μm). d PTP1B inhibition either by shRNAs or by LXQ46 increased the phosphorylation of PKM2. e, f The inactivated PKM2 resulted in increased phosphorylation of AMPKα and decreased the phosphorylation of PRAS40, causing the inhibition of mTOC1 activity. g PTP1B inhibition caused AMPK activation and decreased p-p70S6K in vivo (scale bar, 200 and 50 μm).

5). Exosomes derived from miR-26a-modified MSCs promote axonal regeneration via the PTEN/AKT/mTOR pathway following spinal cord injury. Stem Cell Research & Therapy, 2021 (PubMed: 33820561) [IF=7.5]

Application: WB Species: rat Sample: PC16 cells

FIGURE S2 | miR-26a-overexpressing exosomes inhibited autophagic activity and promoted axonal generation in PC12 cells. (a) The ability of Exos-26a to generate neurofilament (red fluorescent dye) in PC12 cells, which could be reversed by rapamycin. (b, c) Representative images of western blots used to determine the expression levels of NF, mTOR, p-mTOR, AMPK, p-AMPK, S6K, p-S6K, ULK1, p-ULK1, and p62 and semiquantification of the data. RAP indicates miR-26a exosome and rapamycin (100 nM) treatment for 48 h before lysis. *P < 0.05, **P < 0.01, ***P < 0.001 compared with the control group by t test or ANOVA. #P < 0.05 and ##P < 0.01 compared with the RAP group by t test. n = 3 for each group.

6). Timosaponin BII improved osteoporosis caused by hyperglycemia through promoting autophagy of osteoblasts via suppressing the mTOR/NFκB signaling pathway. Free Radical Biology and Medicine, 2021 (PubMed: 33992678) [IF=7.1]

Application: WB Species: Rat Sample: osteoblasts

Fig. 5. Timosaponin BII downregulated mTOR signaling in tibias of diabetic rats and in the high glucose-induced osteoblasts. A: Photomicrographs of the immunohistochemistry staining ( × 200, scale bar: 100 μm; × 400, scale bar: 50 μm) and the quantification of the p-mTOR expression in tibias of different groups of rats. Error bars indicated SEM (n = 6). **P < 0.01 compared with the Mod group. The arrows denoted positive staining. B: Representative western blot images and the quantification of p-mTOR, mTOR, p-S6K and S6K expression in the high glucose-induced osteoblasts with the treatment with TBII (0.1 μmol/L, 1 μmol/L, 10 μmol/L) and in those cells with NAC (25 μmol/L) incubation for 48 h **P < 0.01 compared with the high glucose group.

7). Patchouli alcohol protects against chronic unpredictable mild stress-induced depressant-like behavior through inhibiting excessive autophagy via activation of mTOR signaling pathway. BIOMEDICINE & PHARMACOTHERAPY, 2020 (PubMed: 32244196) [IF=6.9]

Application: WB Species: rat Sample: hippocampus

Fig. 5.| The effect of PA on the level of expression of p-p70S6K protein in the hippocampus. (A) The effect of PA on p-p70S6K and p70S6K protein levels in hippocampus were investigated by western blot analysis.

8). Design, Synthesis, and Biological Evaluation of Imidazo[1,2-a]pyridine Derivatives as Novel PI3K/mTOR Dual Inhibitors. JOURNAL OF MEDICINAL CHEMISTRY, 2020 (PubMed: 32069401) [IF=6.8]

Application: WB Species: Human Sample: HCT116 and HT-29 cells

Figure 5. Effects of 15a on pAKT, AKT, p-p70S6K, and p70S6K in HCT116 and HT-29 cells. HCT116 cells and HT-29 cells were treated at the indicated concentrations of 15a for 24 h. The expression levels of AKT, p70S6K, and their phosphorylated forms were analyzed by Western blotting. GAPDH was used as a loading control.

9). PPM1H is down-regulated by ATF6 and dephosphorylates p-RPS6KB1 to inhibit progression of hepatocellular carcinoma. Molecular therapy. Nucleic acids, 2023 (PubMed: 37456776) [IF=6.5]

Application: WB Species: Human Sample: Hep-G2 cells

Figure 4. PPM1H directly dephosphorylated p-RPS6KB1 A–C) 24 h after transfection, cells were cultured in basal medium without serum overnight; insulin (10 ng/μL) was added 2 h before harvest to activate phosphorylation of RPS6KB1. (A) FLAG-PPM1H was transfected into Hep-G2 cells with or without insulin treatment, and coIP was performed to examine the level of RPS6KB1 combined with PPM1H. (B) CoIP analysis of PPM1H and RPS6KB1 in FLAG-RPS6KB1-transfected Hep-G2 cells with or without insulin treatment. (C) Western blot analysis of the indicated protein levels in PPM1H-overexpressing Hep-G2 cells with or without insulin treatment. (D) In vitro phosphatase assay to determine the interaction between PPM1H and p-RPS6KB1. (E and F) Western blot analysis of the indicated protein levels in vector, ATF6, sh-NC, and sh-ATF6 transfected Hep-G2 cells (E) and in liver tissues of Atf6fl/fl or Atf6Δhep mice. (G) The RPS6KB1 inhibitor PF-4708671 was added to cells at a concentration of 10 μM, which effectively blocked phosphorylation of p-RPS6KB1. Transwell assays revealed that the migration and invasion of PF-4708671-treated Hep-G2 and Huh-7 cells showed little difference between vector and PPM1H. Magnification, ×100. (H) Quantification of (G). Data represent the mean ± SD of three independent experiments. ns, not significant.

10). Dietary sanguinarine supplementation recovers the decrease in muscle quality and nutrient composition induced by high-fat diets of grass carp (Ctenopharyngodon idella). Animal nutrition (Zhongguo xu mu shou yi xue hui), 2024 (PubMed: 38800733) [IF=6.1]

Application: WB Species: fish Sample:

Fig. 5 The effects of different diets on muscle protein synthesis and lipolysis of grass carp. (A) Protein synthesis related gene expression; (B) lipolysis-related gene expression; (C) Western blot analysis of p-AMPK, AMPK, PPARα, TOR, p70S6K, PI3K, and AKT protein expression; (D) relative quantification of p-AMPK, PPARα, TOR, p70S6K, PI3K, and AKT protein expression. The bars indicate the mean ± standard error (SE). Different superscripts denote significant differences (P < 0.05). CON = a control group (containing 4.95% crude fat); HFD = a high fat diet (containing 10.27% crude fat); HFDS = supplementing 1200 μg/kg sanguinarine to HFD.

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p70 S6 Kinase Antibody - #AF6226

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