- Featured Product
- KD/KO Validated
C6orf150 Polyclonal Antibody for IF, WB, ELISA
Cat no : 26416-1-AP
C6orf150, cGAS, Cyclic GMP-AMP synthase, h-cGAS, MB21D1
|Positive WB detected in||HL-60 cells, THP-1 cells|
|Positive IF detected in||HeLa cells|
|Western Blot (WB)||WB : 1:1000-1:4000|
|Immunofluorescence (IF)||IF : 1:20-1:200|
|Sample-dependent, check data in validation data gallery|
The 26416-1-AP immunogen is Fusion Protein C6orf150 protein expressed in E. coli.
|Host / Isotype||Rabbit / IgG|
|Immunogen||C6orf150 fusion protein Ag23455|
|Full Name||chromosome 6 open reading frame 150|
|Calculated molecular weight||496aa, 54 kDa|
|Observed molecular weight||58 kDa|
|GenBank accession number||BC113608|
|Gene ID (NCBI)||115004|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.1% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
cGAS (Cyclic GMP-AMP synthase), also known as C6orf150 or h-cGAS, is a 522 aa protein. cGAS mediates innate immune responses against invading pathogens, or against self-dsDNA, which causes autoimmune disorders. The cGAS sensor not only recognizes cytosolic dsDNA but also synthesizes the second messenger cGAMP from ATP and GTP, which then binds to and activates STING. STING undergoes conformational changes and translocation from the endoplasmic reticulum to the Golgi apparatus to encounter TBK1 and IRF3, eventually triggering the production of type I IFNs.
IFI16 regulates HTLV-1 replication through promoting HTLV-1 RTI-induced innate immune responses.
mTOR Dysregulation by Vaccinia Virus F17 Controls Multiple Processes with Varying Roles in Infection.
Restriction of HCMV replication by ISG15, a host effector regulated by cGAS-STING dsDNA sensing.
HLA-DMB restricts human T-cell leukemia virus type-1 (HTLV-1) protein expression via regulation of ATG7 acetylation.
Ku70 Senses HTLV-1 DNA and Modulates HTLV-1 Replication.
BRD4 inhibition exerts anti-viral activity through DNA damage-dependent innate immune responses.