97久久久精品综合88久久_亚洲国产精品一_久热热国产久热_97操操操_北条麻妃在线免费观看_精品国自产拍天天拍

掃碼關(guān)注公眾號(hào)           掃碼咨詢技術(shù)支持           掃碼咨詢技術(shù)服務(wù)
  
客服熱線:400-901-9800  客服QQ:4009019800  技術(shù)答疑  技術(shù)支持  質(zhì)量反饋  關(guān)于我們  聯(lián)系我們
中文字幕av久久激情亚洲精品,夜夜躁狠狠躁2021,搡女人真爽免费视频大全
Rabbit Anti-phospho-FGFR3 (Tyr724)/Gold Conjugated antibody (bs-13170R-Gold)
訂購(gòu)熱線:400-901-9800
訂購(gòu)郵箱:sales@bioss.com.cn
訂購(gòu)QQ:  400-901-9800
技術(shù)支持:techsupport@bioss.com.cn
說 明 書: 100ul(10nm  15nm  35nm
100ul/2980.00元
大包裝/詢價(jià)
產(chǎn)品編號(hào) bs-13170R-Gold
英文名稱 Rabbit Anti-phospho-FGFR3 (Tyr724)/Gold Conjugated antibody
中文名稱 膠體金標(biāo)記的磷酸化成纖維細(xì)胞生長(zhǎng)因子受體3抗體
別    名 FGFR3 (phospho Y724); FGFR3 (phospho Tyr724); p-FGFR3 (phospho Y724); ACH; CD 333; CD333; CD333 antigen; CEK 2; CEK2; FGFR 3; Fibroblast growth factor receptor 3 (achondroplasia thanatophoric dwarfism); Fibroblast growth factor receptor 3; Heparin binding growth factor receptor; HSFGFR3EX; Hydroxyaryl protein kinase; JTK 4; JTK4; MFR 3; SAM 3; Tyrosine kinase JTK 4; Tyrosine kinase JTK4; Z FGFR 3.  
規(guī)格價(jià)格 100ul/2980元 購(gòu)買        大包裝/詢價(jià)
說 明 書 100ul(10nm  15nm  35nm
產(chǎn)品類型 磷酸化抗體 
研究領(lǐng)域 腫瘤  細(xì)胞生物  信號(hào)轉(zhuǎn)導(dǎo)  生長(zhǎng)因子和激素  轉(zhuǎn)錄調(diào)節(jié)因子  細(xì)胞膜受體  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) (predicted: Human, Mouse, Rat, Dog, Cow, Horse, Rabbit, Sheep, )
產(chǎn)品應(yīng)用 IEM=1:20-200 ICA=1:20-200 ChIP=1:20-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 86kDa
性    狀 Lyophilized or Liquid
濃    度 0.4mg/ml
免 疫 原 KLH conjugated synthesised phosphopeptide derived from human FGFR3 around the phosphorylation site of Tyr724
亞    型 IgG
純化方法 affinity purified by Protein A
儲(chǔ) 存 液 0.02M TBS(pH8.2) with 1% BSA, 0.03% Proclin300.
保存條件 Store at 2-8 oC for 3-6 months. Avoid repeated freeze/thaw cycles.
產(chǎn)品介紹 background:
The encoded protein is synthesized mainly in corticotroph cells of the anterior pituitary where four cleavage sites are used; adrenocorticotrophin, essential for normal steroidogenesis and the maintenance of normal adrenal weight, and lipotropin beta are the major end products. In other tissues, including the hypothalamus, placenta, and epithelium, all cleavage sites may be used, giving rise to peptides with roles in pain and energy homeostasis, melanocyte stimulation, and immune modulation. These include several distinct melanotropins, lipotropins, and endorphins that are contained within the adrenocorticotrophin and beta-lipotropin peptides. Mutations in this gene have been associated with early onset obesity, adrenal insufficiency, and red hair pigmentation. Alternatively spliced transcript variants encoding the same protein have been described.

Function:
Tyrosine-protein kinase that acts as cell-surface receptor for fibroblast growth factors and plays an essential role in the regulation of cell proliferation, differentiation and apoptosis. Plays an essential role in the regulation of chondrocyte differentiation, proliferation and apoptosis, and is required for normal skeleton development. Regulates both osteogenesis and postnatal bone mineralization by osteoblasts. Promotes apoptosis in chondrocytes, but can also promote cancer cell proliferation. Required for normal development of the inner ear. Phosphorylates PLCG1, CBL and FRS2. Ligand binding leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate.

Subunit:
Monomer. Homodimer after ligand binding. Interacts with FGF1, FGF2, FGF4, FGF6; FGF8, FGF9, FGF10, FGF17, FGF18, FGF19, FGF20 and FGF23 (in vitro). Interacts with KLB. Affinity for fibroblast growth factors (FGFs) is increased by heparan sulfate glycosaminoglycans that function as coreceptors. Likewise, KLB increases the affinity for FGF19 and FGF21. Interacts with PIK3R1, PLCG1, SOCS1 and SOCS3.

Subcellular Location:
Cell membrane; Single-pass type I membrane protein. Cytoplasmic vesicle. Endoplasmic reticulum. Note=The activated receptor is rapidly internalized and degraded. Detected in intracellular vesicles after internalization of the autophosphorylated receptor.

Tissue Specificity:
Expressed in brain, kidney and testis. Very low or no expression in spleen, heart, and muscle. In 20- to 22-week old fetuses it is expressed at high level in kidney, lung, small intestine and brain, and to a lower degree in spleen, liver, and muscle. Isoform 2 is detected in epithelial cells. Isoform 1 is not detected in epithelial cells. Isoform 1 and isoform 2 are detected in fibroblastic cells.

Post-translational modifications:
Autophosphorylated. Binding of FGF family members together with heparan sulfate proteoglycan or heparin promotes receptor dimerization and autophosphorylation on tyrosine residues. Autophosphorylation occurs in trans between the two FGFR molecules present in the dimer. Phosphorylation at Tyr-724 is essential for stimulation of cell proliferation and activation of PIK3R1, STAT1 and MAP kinase signaling. Phosphorylation at Tyr-760 is required for interaction with PIK3R1 and PLCG1.

DISEASE:
Defects in FGFR3 are the cause of achondroplasia (ACH) [MIM:100800]. ACH is an autosomal dominant disease and is the most frequent form of short-limb dwarfism. It is characterized by a long, narrow trunk, short extremities, particularly in the proximal (rhizomelic) segments, a large head with frontal bossing, hypoplasia of the midface and a trident configuration of the hands.
Defects in FGFR3 are the cause of Crouzon syndrome with acanthosis nigricans (CAN) [MIM:612247]. Classic Crouzon disease which is caused by mutations in the FGFR2 gene is characterized by craniosynostosis (premature fusion of the skull sutures), and facial hypoplasia. Crouzon syndrome with acanthosis nigricans (a skin disorder characterized by pigmentation anomalies), CAN, is considered to be an independent disorder from classic Crouzon syndrome. CAN is characterized by additional more severe physical manifestation, such as Chiari malformation, hydrocephalus, and atresia or stenosis of the choanas, and is caused by a specific mutation (Ala-391 to Glu) in the transmembrane domain of FGFR3. It is proposed to have an autosomal dominant mode of inheritance.
Defects in FGFR3 are a cause of thanatophoric dysplasia type 1 (TD1) [MIM:187600]; also known as thanatophoric dwarfism or platyspondylic lethal skeletal dysplasia Sand Diego type (PLSD-SD). TD1 is the most common neonatal lethal skeletal dysplasia. Affected individuals display features similar to those seen in homozygous achondroplasia. It causes severe shortening of the limbs with macrocephaly, narrow thorax and short ribs. In the most common subtype, TD1, femur are curved.
Defects in FGFR3 are a cause of thanatophoric dysplasia type 2 (TD2) [MIM:187601]. It is a neonatal lethal skeletal dysplasia causing severe shortening of the limbs, narrow thorax and short ribs. Patients with thanatophoric dysplasia type 2 have straight femurs and cloverleaf skull.
Defects in FGFR3 are a cause of hypochondroplasia (HCH) [MIM:146000]. HCH is an autosomal dominant disease and is characterized by disproportionate short stature. It resembles achondroplasia, but with a less severe phenotype.
Defects in FGFR3 are a cause of susceptibility to bladder cancer (BLC) [MIM:109800]. A malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and at different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences. Note=Somatic mutations can constitutively activate FGFR3.
Defects in FGFR3 are a cause of cervical cancer (CERCA) [MIM:603956]. A malignant neoplasm of the cervix, typically originating from a dysplastic or premalignant lesion previously present at the active squamocolumnar junction. The transformation from mild dysplastic to invasive carcinoma generally occurs slowly within several years, although the rate of this process varies widely. Carcinoma in situ is particularly known to precede invasive cervical cancer in most cases. Cervical cancer is strongly associated with infection by oncogenic types of human papillomavirus.

Similarity:
Belongs to the protein kinase superfamily. Tyr protein kinase family.
Fibroblast growth factor receptor subfamily.
Contains 3 Ig-like C2-type (immunoglobulin-like) domains.
Contains 1 protein kinase domain.

Database links:

Entrez Gene: 2261 Human

Entrez Gene: 14184 Mouse

Entrez Gene: 84489 Rat

Omim: 134934 Human

SwissProt: P22607 Human

SwissProt: Q61851 Mouse

Unigene: 1420 Human

Unigene: 6904 Mouse

Unigene: 23671 Rat



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
版權(quán)所有 2004-2026 www.kastlife.cn 北京博奧森生物技術(shù)有限公司
通過國(guó)際質(zhì)量管理體系ISO 9001:2015 GB/T 19001-2016    證書編號(hào): 00124Q34771R2M/1100
通過國(guó)際醫(yī)療器械-質(zhì)量管理體系ISO 13485:2016 GB/T 42061-2022    證書編號(hào): CQC24QY10047R0M/1100
京ICP備05066980號(hào)-1         京公網(wǎng)安備110107000727號(hào)
主站蜘蛛池模板: 香蕉97超级碰碰碰视频 | 中文字幕亚洲精品无码 | 操草视频| 欧美性受ⅹ╳╳╳黑人a性爽 | 欧美片网站免费 | 无码人妻精品一区二区在线视频 | 国产偷久久一级精品av小说 | 狼群社区WWW在线中文 | japanese乱子xxxx| 九九在线中文字幕无码 | 久久精品99久久 | 加勒比无码专区中文字幕 | 国产秋霞理论久久久 | 成人av中文解说水果派在线观看 | www.综合久久 | 国产性网 | 国产精品第一页爽爽影院 | 国产二区久久 | 一区二区视频免费 | 国产A∨天天免费观看美女 亚洲精品7777 | av在线亚洲天堂 | 99视频在线精品 | 多人调教到高潮失禁h重口文 | 国产精品日韩欧美一区二区 | 大地资源在线观看视频 | 久久久激情综合 | 黄色一级在线视频 | 国产精品日韩AV在线播放 | 亚洲在线免费视频 | 人妻系列无码专区久久五月天 | 五月丁香六月激情综合在线视频 | 亚洲第一网站男人都懂 | 日韩欧美大片在线观看 | 特大巨黑吊xxx | 一道本一区二区三区 | 丰满少妇xbxb毛片日本视频 | 日本三级吃奶头添泬 | 一区二区精品视频 | HTTPWWW色午夜COM曰本 | 亚洲日韩欧美内射教官 | 国产高清一级毛片在线不卡 |