Product Name	KRIT1
Chinese Name	脑海绵状血管畸形蛋白1抗体
Alias	Ankyrin repeat containing protein Krit1; CAM; CCM 1; CCM1; Cerebral cavernous malformations 1; Cerebral cavernous malformations 1 protein; Krev interaction trapped 1; Krev interaction trapped protein 1; KRIT 1; KRIT1 ankyrin repeat containing; KRIT1; KRIT1_HUMAN.
Research Area	Cardiovascular  Neurobiology  Signal transduction  G protein-coupled receptor  vascular endothelial cell
Immunogen Species	Rabbit
Clonality	Polyclonal
React Species	Mouse,  (predicted: Human, Rat, Chicken, Dog, Pig, Cow, Horse, Rabbit, )
Applications	WB=1:500-2000 ELISA=1:5000-10000  not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
Theoretical molecular weight	84kDa
Cellular localization	The cell membrane
Form	Liquid
Concentration	1mg/ml
immunogen	KLH conjugated synthetic peptide derived from human KRIT1: 631-736/736
Lsotype	IgG
Purification	affinity purified by Protein A
Buffer Solution	0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
Storage	Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
Attention	This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed	PubMed
Product Detail	Negative regulator of angiogenesis. Inhibits endothelial proliferation, apoptosis, migration, lumen formation and sprouting angiogenesis in primary endothelial cells. Promotes AKT phosphorylation in a NOTCH-dependent and independent manner, and inhibits EKR1/2 phosphorylation indirectly through activation of the DELTA-NOTCH cascade. Acts in concert with CDH5 to establish and maintain correct endothelial cell polarity and vascular lumen and these effects are mediated by recruitment and activation of the Par polarity complex and RAP1B. Required for the localization of phosphorylated PRKCZ, PARD3, TIAM1 and RAP1B to the cell junction. Plays an important role in the maintenance of the intracellular reactive oxygen species (ROS) homeostasis to prevent oxidative cellular damage. Regulates the homeostasis of intracellular ROS through an antioxidant pathway involving FOXO1 and SOD2. Facilitates the down-regulation of cyclin D1 levels required for cell transition from proliferative growth to quiescence by preventing the accumulation of intracellular ROS through the modulation of FOXO1 and SOD2 levels. Function: Component of the CCM signaling pathway which is a crucial regulator of heart and vessel formation and integrity (By similarity). Negative regulator of angiogenesis. Inhibits endothelial proliferation, apoptosis, migration, lumen formation and sprouting angiogenesis in primary endothelial cells. Promotes AKT phosphorylation in a NOTCH-dependent and independent manner, and inhibits EKR1/2 phosphorylation indirectly through activation of the DELTA-NOTCH cascade. Acts in concert with CDH5 to establish and maintain correct endothelial cell polarity and vascular lumen and these effects are mediated by recruitment and activation of the Par polarity complex and RAP1B. Required for the localization of phosphorylated PRKCZ, PARD3, TIAM1 and RAP1B to the cell junction. Plays an important role in the maintenance of the intracellular reactive oxygen species (ROS) homeostasis to prevent oxidative cellular damage. Regulates the homeostasis of intracellular ROS through an antioxidant pathway involving FOXO1 and SOD2. Facilitates the down-regulation of cyclin-D1 (CCND1) levels required for cell transition from proliferative growth to quiescence by preventing the accumulation of intracellular ROS through the modulation of FOXO1 and SOD2 levels. Subunit: Interacts with RAP1A. Interacts with CDH5. Interacts with HEG1 and CCM2; greatly facilitates CCM2-binding to HEG1 (By similarity). Subcellular Location: Membrane. Cell junction. KRIT1 and CDH5 reciprocally regulate their localization to endothelial cell-cell junctions. Tissue Specificity: Low levels in brain. Very weak expression found in heart and muscle. DISEASE: Involvement in disease;Defects in KRIT1 are the cause of cerebral cavernous malformations type 1 (CCM1). Cerebral cavernous malformations (CCMs) are congenital vascular anomalies of the central nervous system that can result in hemorrhagic stroke, seizures, recurrent headaches, and focal neurologic deficits. CCMs have an incidence of 0.1%-0.5% in the general population and usually present clinically during the 3rd to 5th decade of life. The lesions are characterized by grossly enlarged blood vessels consisting of a single layer of endothelium and without any intervening neural tissue, ranging in diameter from a few millimeters to several centimeters. Similarity: Contains 4 ANK repeats. Contains 1 FERM domain. SWISS: O00522 Gene ID: 889 Database links: Entrez Gene: 889 Human Entrez Gene: 79264 Mouse Entrez Gene: 362317 Rat Omim: 604214 Human SwissProt: Q6TNJ1 Cow SwissProt: O00522 Human SwissProt: Q6S5J6 Mouse Unigene: 531987 Human Unigene: 32368 Mouse Unigene: 482273 Mouse
Product Picture	Sample: Heart (Mouse) Lysate at 40 ug Primary: Anti- KRIT1 (SL8546R) at 1/1000 dilution Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution Predicted band size: 84 kD Observed band size: 80 kD

Cartpieces

• 
• 9

  9Delete

• 
• 5

  5Delete

• 
• S

  SDelete

• 
• R

  RDelete

• 
• +

  +Delete

• 
• 2

  2Delete

• Delete

• Delete

• 
• 1

  1Delete

• 
• 1

  1Delete

• 
• $

  $Delete

• 
• 0

  0Delete

• 
• 4

  4Delete

• 
• $

  $Delete

• 
• 0

  0Delete

• 
• 0

  0Delete

• 
• 1

  1Delete

• 
• A

  ADelete

• 
• A

  ADelete

• 

• Delete

• 
• i

  iDelete

• 
• i

  iDelete

• Delete

• 
• 1

  1Delete

• Delete

• 
• 1

  1Delete

• 
• 1

  1Delete

• 
• 0

  0Delete

• Delete

• 
• 2

  2Delete

• 
• 1

  1Delete

• 
• 0

  0Delete

• 
• 0

  0Delete

• 
• 0

  0Delete

• 
• 0

  0Delete

• 
• 0

  0Delete

• 
• 0

  0Delete

• 
• 1

  1Delete

• 
• 1

  1Delete

• Delete

• 
• -

  -Delete

• 
• -

  -Delete

• 
• 0

  0Delete

• Delete

• 
• t

  tDelete

• 
• 0

  0Delete

• 
• 0

  0Delete

• 
• 0

  0Delete

• 
• f

  fDelete

• Delete

• Delete

• Delete

• Delete

• Delete

• Delete

• Delete

• Delete

• Delete

• Delete

• Delete

• Delete

• Delete

• Delete

• 
• 4

  4Delete

• 
• $

  $Delete

• Delete

• 
• 0

  0Delete

• Delete

• Delete

• Delete

• 
• R

  RDelete

• 
• 5

  5Delete

• 
• A

  ADelete

Totalgoods,subtotals:￥Checkout