Human MAN1B1 activation kit by CRISPRa

CAT#: GA107754

MAN1B1 CRISPRa kit - CRISPR gene activation of human mannosidase alpha class 1B member 1



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CNY 12,255.00


货期*
4周

规格
    • 1 kit

Product images

经常一起买 (2)
MAN1B1 rabbit polyclonal antibody
    • 100 ul

CNY 1,999.00
CNY 3,280.00


MAN1B1 (Myc-DDK-tagged)-Human mannosidase, alpha, class 1B, member 1 (MAN1B1)
    • 10 ug

CNY 5,120.00
CNY 5,800.00

Specifications

Product Data
Format 3 gRNAs (5ug each), 1 scramble ctrl (10ug) and 1 enhancer vector (10ug)
Symbol MAN1B1
Locus ID 11253
Kit Components

GA107754G1, MAN1B1 gRNA vector 1 in pCas-Guide-GFP-CRISPRa

GA107754G2, MAN1B1 gRNA vector 2 in pCas-Guide-GFP-CRISPRa

GA107754G3, MAN1B1 gRNA vector 3 in pCas-Guide-GFP-CRISPRa

1 CRISPRa-Enhancer vector, SKU GE100056

1 CRISPRa scramble vector, SKU GE100077

Disclaimer These products are manufactured and supplied by OriGene under license from ERS. The kit is designed based on the best knowledge of CRISPRa SAM technology. The efficiency of the activation can be affected by many factors, including nucleosome occupancy status, chromatin structure and the gene expression level of the target, etc.
Reference Data
RefSeq NM_007230, NM_016219, NR_045720, NR_045721
Synonyms DKFZP434I213; MANA-ER
Summary This gene encodes an enzyme belonging to the glycosyl hydrolase 47 family. This enzyme functions in N-glycan biosynthesis, and is a class I alpha-1,2-mannosidase that specifically converts Man9GlcNAc to Man8GlcNAc isomer B. It is required for N-glycan trimming to Man5-6GlcNAc2 in the endoplasmic-reticulum-associated degradation pathway. Mutations in this gene cause autosomal-recessive intellectual disability. Alternative splicing results in multiple transcript variants. A related pseudogene has been identified on chromosome 11. [provided by RefSeq, Dec 2011]
*Delivery time may vary from web posted schedule. Occasional delays may occur due to unforeseen complexities in the preparation of your product. International customers may expect an additional 1-2 weeks in shipping.

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