Name | Number of supported studies | Average coverage | |
---|---|---|---|
plasmacytoid dendritic cell | 5 studies | 18% ± 3% | |
natural killer cell | 3 studies | 21% ± 4% | |
classical monocyte | 3 studies | 20% ± 3% | |
dendritic cell | 3 studies | 21% ± 4% |
Insufficient scRNA-seq data for expression of CGAS at tissue level.
Tissue | GTEx Coverage | GTEx Average TPM | GTEx Number of samples | TCGA Coverage | TCGA Average TPM | TCGA Number of samples |
---|---|---|---|---|---|---|
esophagus | 100% | 251.27 | 1438 / 1445 | 97% | 18.98 | 177 / 183 |
uterus | 100% | 335.49 | 170 / 170 | 96% | 18.28 | 441 / 459 |
breast | 100% | 290.80 | 459 / 459 | 95% | 8.43 | 1062 / 1118 |
lung | 99% | 553.82 | 575 / 578 | 94% | 12.22 | 1087 / 1155 |
stomach | 97% | 179.75 | 349 / 359 | 95% | 11.22 | 273 / 286 |
intestine | 100% | 310.95 | 965 / 966 | 91% | 9.35 | 478 / 527 |
bladder | 100% | 364.05 | 21 / 21 | 90% | 10.67 | 456 / 504 |
thymus | 100% | 276.34 | 651 / 653 | 89% | 4.21 | 537 / 605 |
ovary | 98% | 186.67 | 177 / 180 | 87% | 7.29 | 376 / 430 |
prostate | 100% | 323.60 | 245 / 245 | 81% | 3.21 | 407 / 502 |
pancreas | 81% | 100.42 | 265 / 328 | 96% | 8.92 | 170 / 178 |
kidney | 91% | 143.88 | 81 / 89 | 68% | 3.48 | 617 / 901 |
skin | 79% | 194.08 | 1427 / 1809 | 72% | 5.26 | 341 / 472 |
adrenal gland | 95% | 129.69 | 245 / 258 | 28% | 1.17 | 64 / 230 |
brain | 76% | 101.51 | 2008 / 2642 | 40% | 1.92 | 283 / 705 |
adipose | 100% | 389.69 | 1204 / 1204 | 0% | 0 | 0 / 0 |
lymph node | 0% | 0 | 0 / 0 | 100% | 16.61 | 29 / 29 |
spleen | 100% | 824.12 | 241 / 241 | 0% | 0 | 0 / 0 |
tonsil | 0% | 0 | 0 / 0 | 100% | 22.49 | 45 / 45 |
ureter | 0% | 0 | 0 / 0 | 100% | 5.84 | 1 / 1 |
peripheral blood | 99% | 941.89 | 924 / 929 | 0% | 0 | 0 / 0 |
blood vessel | 99% | 268.80 | 1326 / 1335 | 0% | 0 | 0 / 0 |
heart | 85% | 142.49 | 733 / 861 | 0% | 0 | 0 / 0 |
liver | 49% | 47.31 | 110 / 226 | 24% | 1.31 | 99 / 406 |
muscle | 24% | 22.38 | 192 / 803 | 0% | 0 | 0 / 0 |
eye | 0% | 0 | 0 / 0 | 19% | 0.62 | 15 / 80 |
abdomen | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
bone marrow | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
diaphragm | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
gingiva | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
nasal cavity | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
nasopharynx | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
nose | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
placenta | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
spinal column | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
GO_0019934 | Biological process | cGMP-mediated signaling |
GO_0006281 | Biological process | DNA repair |
GO_0002221 | Biological process | pattern recognition receptor signaling pathway |
GO_2000774 | Biological process | positive regulation of cellular senescence |
GO_0045087 | Biological process | innate immune response |
GO_0008340 | Biological process | determination of adult lifespan |
GO_0051607 | Biological process | defense response to virus |
GO_0006974 | Biological process | DNA damage response |
GO_0038001 | Biological process | paracrine signaling |
GO_0019933 | Biological process | cAMP-mediated signaling |
GO_0160049 | Biological process | negative regulation of cGAS/STING signaling pathway |
GO_0032481 | Biological process | positive regulation of type I interferon production |
GO_0002637 | Biological process | regulation of immunoglobulin production |
GO_2000042 | Biological process | negative regulation of double-strand break repair via homologous recombination |
GO_0140896 | Biological process | cGAS/STING signaling pathway |
GO_0050863 | Biological process | regulation of T cell activation |
GO_0002218 | Biological process | activation of innate immune response |
GO_0071360 | Biological process | cellular response to exogenous dsRNA |
GO_0002230 | Biological process | positive regulation of defense response to virus by host |
GO_0002753 | Biological process | cytoplasmic pattern recognition receptor signaling pathway |
GO_0005886 | Cellular component | plasma membrane |
GO_0005654 | Cellular component | nucleoplasm |
GO_0016604 | Cellular component | nuclear body |
GO_0005829 | Cellular component | cytosol |
GO_0005737 | Cellular component | cytoplasm |
GO_0035861 | Cellular component | site of double-strand break |
GO_0005634 | Cellular component | nucleus |
GO_0003677 | Molecular function | DNA binding |
GO_0042803 | Molecular function | protein homodimerization activity |
GO_0160004 | Molecular function | poly-ADP-D-ribose modification-dependent protein binding |
GO_0003682 | Molecular function | chromatin binding |
GO_0003690 | Molecular function | double-stranded DNA binding |
GO_0005546 | Molecular function | phosphatidylinositol-4,5-bisphosphate binding |
GO_0005525 | Molecular function | GTP binding |
GO_0140693 | Molecular function | molecular condensate scaffold activity |
GO_0046872 | Molecular function | metal ion binding |
GO_0005524 | Molecular function | ATP binding |
GO_0061501 | Molecular function | 2',3'-cyclic GMP-AMP synthase activity |
GO_0031491 | Molecular function | nucleosome binding |
GO_0005515 | Molecular function | protein binding |
Gene name | CGAS |
Protein name | Cyclic GMP-AMP synthase Cyclic GMP-AMP synthase (cGAMP synthase) (cGAS) (h-cGAS) (EC 2.7.7.86) (2'3'-cGAMP synthase) (Mab-21 domain-containing protein 1) |
Synonyms | C6orf150 MB21D1 |
Description | FUNCTION: Nucleotidyltransferase that catalyzes the formation of cyclic GMP-AMP (2',3'-cGAMP) from ATP and GTP and plays a key role in innate immunity . Catalysis involves both the formation of a 2',5' phosphodiester linkage at the GpA step and the formation of a 3',5' phosphodiester linkage at the ApG step, producing c[G(2',5')pA(3',5')p] . Acts as a key DNA sensor: directly binds double-stranded DNA (dsDNA), inducing the formation of liquid-like droplets in which CGAS is activated, leading to synthesis of 2',3'-cGAMP, a second messenger that binds to and activates STING1, thereby triggering type-I interferon production . Preferentially recognizes and binds curved long dsDNAs of a minimal length of 40 bp . Acts as a key foreign DNA sensor, the presence of double-stranded DNA (dsDNA) in the cytoplasm being a danger signal that triggers the immune responses . Has antiviral activity by sensing the presence of dsDNA from DNA viruses in the cytoplasm . Also acts as an innate immune sensor of infection by retroviruses, such as HIV-2, by detecting the presence of reverse-transcribed DNA in the cytosol . In contrast, HIV-1 is poorly sensed by CGAS, due to its capsid that cloaks viral DNA from CGAS detection . Detection of retroviral reverse-transcribed DNA in the cytosol may be indirect and be mediated via interaction with PQBP1, which directly binds reverse-transcribed retroviral DNA . Also detects the presence of DNA from bacteria, such as M.tuberculosis . 2',3'-cGAMP can be transferred from producing cells to neighboring cells through gap junctions, leading to promote STING1 activation and convey immune response to connecting cells . 2',3'-cGAMP can also be transferred between cells by virtue of packaging within viral particles contributing to IFN-induction in newly infected cells in a cGAS-independent but STING1-dependent manner . Also senses the presence of neutrophil extracellular traps (NETs) that are translocated to the cytosol following phagocytosis, leading to synthesis of 2',3'-cGAMP . In addition to foreign DNA, can also be activated by endogenous nuclear or mitochondrial DNA . When self-DNA leaks into the cytosol during cellular stress (such as mitochondrial stress, SARS-CoV-2 infection causing severe COVID-19 disease, DNA damage, mitotic arrest or senescence), or is present in form of cytosolic micronuclei, CGAS is activated leading to a state of sterile inflammation . Acts as a regulator of cellular senescence by binding to cytosolic chromatin fragments that are present in senescent cells, leading to trigger type-I interferon production via STING1 and promote cellular senescence (By similarity). Also involved in the inflammatory response to genome instability and double-stranded DNA breaks: acts by localizing to micronuclei arising from genome instability . Micronuclei, which are frequently found in cancer cells, consist of chromatin surrounded by their own nuclear membrane: following breakdown of the micronuclear envelope, a process associated with chromothripsis, CGAS binds self-DNA exposed to the cytosol, leading to 2',3'-cGAMP synthesis and subsequent activation of STING1 and type-I interferon production . Activated in response to prolonged mitotic arrest, promoting mitotic cell death . In a healthy cell, CGAS is however kept inactive even in cellular events that directly expose it to self-DNA, such as mitosis, when cGAS associates with chromatin directly after nuclear envelope breakdown or remains in the form of postmitotic persistent nuclear cGAS pools bound to chromatin . Nuclear CGAS is inactivated by chromatin via direct interaction with nucleosomes, which block CGAS from DNA binding and thus prevent CGAS-induced autoimmunity . Also acts as a suppressor of DNA repair in response to DNA damage: inhibits homologous recombination repair by interacting with PARP1, the CGAS-PARP1 interaction leading to impede the formation of the PARP1-TIMELESS complex . In addition to DNA, also sense translation stress: in response to translation stress, translocates to the cytosol and associates with collided ribosomes, promoting its activation and triggering type-I interferon production . In contrast to other mammals, human CGAS displays species-specific mechanisms of DNA recognition and produces less 2',3'-cGAMP, allowing a more fine-tuned response to pathogens . . |
Accessions | Q8N884 ENST00000370318.5 [Q8N884-2] ENST00000370315.4 [Q8N884-1] ENST00000680833.1 A0A7P0TBQ3 |