Product Name	MOCS1
Chinese Name	钼辅因子合成蛋白1抗体
Alias	Cell migration-inducing gene 11 protein; MIG11; MOCOD; Mocs1; MOCS1_HUMAN; Molybdenum cofactor biosynthesis protein 1; Molybdenum cofactor biosynthesis protein A; Molybdenum cofactor biosynthesis protein C; Molybdenum cofactor synthesis 1; Molybdenum cofactor synthesis-step 1 protein A-B.
Research Area	Cell biology  Neurobiology  Signal transduction  The new supersedes the old
Immunogen Species	Rabbit
Clonality	Polyclonal
React Species	(predicted: Human, Mouse, Rat, Pig, Horse, Rabbit, )
Applications	ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:100-500 （Paraffin sections need antigen repair） not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
Theoretical molecular weight	70kDa
Cellular localization	The nucleus cytoplasmic
Form	Liquid
Concentration	1mg/ml
immunogen	KLH conjugated synthetic peptide derived from human MOCS1: 21-120/636
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	Molybdenum cofactor biosynthesis is a conserved pathway leading to the biological activation of molybdenum. The protein encoded by this gene is involved in this pathway. This gene was originally thought to produce a bicistronic mRNA with the potential to produce two proteins (MOCS1A and MOCS1B) from adjacent open reading frames. However, only the first open reading frame (MOCS1A) has been found to encode a protein from the putative bicistronic mRNA, whereas additional splice variants, whose full-length natures have yet to be determined, are likely to produce a fusion between the two open reading frames. This gene is defective in patients with molybdenum cofactor deficiency, type A. A related pseudogene has been identified on chromosome 16. [provided by RefSeq, Jan 2010] Function: Isoform MOCS1A and isoform MOCS1B probably form a complex that catalyzes the conversion of a guanosine derivative to precursor Z during molybdenum cofactor biosynthesis. Tissue Specificity: Isoform MOCS1A and isoform 2 are widely expressed. Post-translational modifications: Isoform MOCS1A, isoform 2 and isoform 3 are probably thiocarboxylated at their C-terminus. Thiocarboxylation probably plays a central role in molybdenum cofactor biosynthesis, since mutagenesis of the last 2 Gly residues of isoform MOCS1A abolishes the catalytic activity of the enzyme. Thiocarboxylation is absent in isoform MOCS1B, which lacks the C-terminal Gly residue. DISEASE: Defects in MOCS1 are the cause of molybdenum cofactor deficiency type A (MOCOD type A) [MIM:252150]; an autosomal recessive disease which leads to the pleiotropic loss of all molybdoenzyme activities and is characterized by severe neurological damage, neonatal seizures and early childhood death. Similarity: In the C-terminal section; belongs to the moaC family. In the N-terminal section; belongs to the moaA/nifB/pqqE family. SWISS: Q9NZB8 Gene ID: 4337 Database links: Entrez Gene: 4337 Human Entrez Gene: 56738 Mouse Entrez Gene: 301221 Rat Omim: 603707 Human SwissProt: Q1JQD7 Cow SwissProt: Q9NZB8 Human SwissProt: Q5RKZ7 Mouse Unigene: 718492 Human Unigene: 22256 Mouse

Cartpieces

• 
• 1

  1Delete

• 
• 5

  5Delete

• 
• S

  SDelete

• 
• R

  RDelete

• 
• +

  +Delete

• 
• 3

  3Delete

• Delete

• Delete

• 
• 1

  1Delete

• 
• 1

  1Delete

• 
• $

  $Delete

• 
• 0

  0Delete

• 
• 4

  4Delete

• 
• $

  $Delete

• 
• 0

  0Delete

• 
• 0

  0Delete

• 
• 1

  1Delete

• 
• C

  CDelete

• 
• C

  CDelete

• 

• 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