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Rabbit Anti-Msx2/Cy7 Conjugated antibody (bs-10158R-Cy7)
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價(jià)
產(chǎn)品編號(hào) bs-10158R-Cy7
英文名稱 Rabbit Anti-Msx2/Cy7 Conjugated antibody
中文名稱 Cy7標(biāo)記的同源盒基因Msx2抗體
別    名 Msx2/Hox8; CRS 2; CRS2; FPP; Homeo box msh like 2; Homeobox protein Hox-8; Homeobox protein MSX 2; Homeobox protein MSX-2; Homeobox protein MSX2; Hox 8; Hox8; MSH; Msh homeo box 2; Msh homeo box homolog; Msh homeo box homolog 2; Msh homeobox 2; Msh homeobox homolog 2; Msx 2; Msx2; MSX2_HUMAN; Parietal foramina 1; PFM 1; PFM; PFM1.  
規(guī)格價(jià)格 100ul/2980元 購買        大包裝/詢價(jià)
說 明 書 100ul  
研究領(lǐng)域 腫瘤  心血管  染色質(zhì)和核信號(hào)  神經(jīng)生物學(xué)  轉(zhuǎn)錄調(diào)節(jié)因子  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) (predicted: Human, Mouse, Rat, Chicken, Dog, Cow, Horse, Rabbit, )
產(chǎn)品應(yīng)用
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 29kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human Msx2/Hox8
亞    型 IgG
純化方法 affinity purified by Protein A
儲(chǔ) 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件 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.
產(chǎn)品介紹 background:
This gene encodes a member of the muscle segment homeobox gene family. The encoded protein is a transcriptional repressor whose normal activity may establish a balance between survival and apoptosis of neural crest-derived cells required for proper craniofacial morphogenesis. The encoded protein may also have a role in promoting cell growth under certain conditions and may be an important target for the RAS signaling pathways. Mutations in this gene are associated with parietal foramina 1 and craniosynostosis type 2. [provided by RefSeq, Jul 2008].

Function:
Acts as a transcriptional regulator in bone development. Represses the ALPL promoter activity and antogonizes the stimulatory effect of DLX5 on ALPL expression during osteoblast differentiation. Probable morphogenetic role. May play a role in limb-pattern formation. In osteoblasts, suppresses transcription driven by the osteocalcin FGF response element (OCFRE). Binds to the homeodomain-response element of the ALPL promoter.

Subunit:
Interacts with MINT. Interacts with XRCC6 (Ku70) and XRCC5 (Ku80).

Subcellular Location:
Nucleus.

DISEASE:
Defects in MSX2 are the cause of parietal foramina 1 (PFM1) [MIM:168500]; also known as foramina parietalia permagna (FPP). PFM1 is an autosomal dominant disease characterized by oval defects of the parietal bones caused by deficient ossification around the parietal notch, which is normally obliterated during the fifth fetal month.
Defects in MSX2 are the cause of parietal foramina with cleidocranial dysplasia (PFMCCD) [MIM:168550]; also known as cleidocranial dysplasia with parietal foramina. PFMCCD combines skull defects in the form of enlarged parietal foramina and deficient ossification of the clavicles.
Defects in MSX2 are the cause of craniosynostosis type 2 (CRS2) [MIM:604757]; also known as craniosynostosis Boston-type (CSB). CRS2 is an autosomal dominant disorder characterized by the premature fusion of calvarial sutures. The craniosynostosis phenotype is either fronto-orbital recession, or frontal bossing, or turribrachycephaly, or cloverleaf skull. Associated features include severe headache, high incidence of visual problems (myopia or hyperopia), and short first metatarsals. Intelligence is normal.

Similarity:
Belongs to the Msh homeobox family.
Contains 1 homeobox DNA-binding domain.

Database links:

Entrez Gene: 4488 Human

Omim: 123101 Human

SwissProt: P35548 Human

Unigene: 89404 Human



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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