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Rabbit Anti-Gliomedin/RBITC Conjugated antibody (bs-11032R-RBITC)
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產品編號 bs-11032R-RBITC
英文名稱 Rabbit Anti-Gliomedin/RBITC Conjugated antibody
中文名稱 羅丹明(RBITC)標記的神經膠質蛋白(肝癌相關基因2)抗體
別    名 CANCER RELATED GENE LIVER 2; Cancer related gene-Liver 2; CLOM; collomin; Colm (gene name); COLM; Colmedin; CRG L2; FLJ23917; Gldn (gene name); UNC 112; GLDN_HUMAN.  
規(guī)格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領域 神經生物學  信號轉導  細胞粘附分子  細胞骨架  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應 Human, Mouse, Rat,  (predicted: Dog, Pig, Cow, Horse, Sheep, )
產品應用 ICC=1:50-200 IF=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 59kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human Gliomedin/COLM
亞    型 IgG
純化方法 affinity purified by Protein A
儲 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.
產品介紹 background:
Gliomedin is a 551 amino acid protein encoded by the human gene GLDN. Gliomedin is thought to play a role in the formation of the nodes of Ranvier along myelinated axons. Accumulation of Na+ channels at the nodes of Ranvier is a prerequisite for saltatory conduction. In peripheral nerves, clustering of these channels along the axolemma is regulated by myelinating Schwann cells through an unknown mechanism. Gliomedin is a glial ligand for Neurofascin and NrCAM, two axonal immunoglobulin cell adhesion molecules that are associated with Na+ channels at the nodes of Ranvier. Gliomedin is expressed by myelinating Schwann cells and accumulates at the edges of each myelin segment during development, where it aligns with the forming nodes. Gliomedin is a single-pass type II membrane protein localized to the nodes of Ranvier and is specifically expressed in spinal cord, brain, placenta and sciatic nerve. It is more abundant in peripheral than central nervous system.

Function:
Gliomedin is a member of the collagen superfamily, it is a glial ligand for neurofascin and NrCAM, two axonal immunoglobulin cell adhesion molecules that are associated with Na+ channels at the nodes of Ranvier. Gliomedin provides a glial cue for the formation of peripheral nodes of Ranvier. Gliomedin is expressed by myelinating Schwann cells and accumulates at the edges of each myelin segment during development, where it aligns with the forming nodes of ranvier. Eliminating the expression of gliomedin or the addition of a soluble extracellular domain of neurofascin to myelinating cultures abolishes node formation. Gliomedin is expressed in the PNS nodes of ranvier, but not in the CNS nodes of ranvier. Gliomedin also displays high expression in murine and human hepatocellular carcinomas (HCC). Its restricted expression in normal tissues and unique early upregulation during tumor development make it an excellent candidate as a new clinical marker of HCC.

Subunit:
Interacts with NFASC/neurofascin and NRCAM.

Subcellular Location:
Cell membrane; Single-pass type II membrane protein. Note=Localizes to the nodes of Ranvier.

Tissue Specificity:
Specifically expressed in spinal cord, brain, placenta and sciatic nerve. More abundant in peripheral than central nervous system.

Similarity:
Contains 2 collagen-like domains.
Contains 1 olfactomedin-like domain.

Database links:

Entrez Gene: 342035 Human

Entrez Gene: 235379 Mouse

Entrez Gene: 315675 Rat

Omim: 608603 Human

SwissProt: Q6ZMI3 Human

SwissProt: Q7Z359 Human

SwissProt: Q80ZC5 Mouse

SwissProt: Q8BMF8 Mouse

SwissProt: Q80WL1 Rat

Unigene: 526441 Human

Unigene: 123549 Mouse

Unigene: 38054 Rat



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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