Name | Number of supported studies | Average coverage | |
---|---|---|---|
epithelial cell | 5 studies | 26% ± 10% | |
astrocyte | 4 studies | 22% ± 5% | |
oligodendrocyte | 4 studies | 18% ± 2% | |
GABAergic neuron | 3 studies | 37% ± 8% | |
glutamatergic neuron | 3 studies | 46% ± 12% | |
dendritic cell | 3 studies | 19% ± 2% | |
basal cell | 3 studies | 17% ± 0% | |
transit amplifying cell | 3 studies | 22% ± 4% |
Tissue | GTEx Coverage | GTEx Average TPM | GTEx Number of samples | TCGA Coverage | TCGA Average TPM | TCGA Number of samples |
---|---|---|---|---|---|---|
esophagus | 100% | 1219.18 | 1445 / 1445 | 100% | 27.15 | 183 / 183 |
brain | 100% | 1194.43 | 2641 / 2642 | 100% | 30.54 | 705 / 705 |
ovary | 100% | 1171.13 | 180 / 180 | 100% | 19.61 | 429 / 430 |
breast | 100% | 1285.53 | 459 / 459 | 100% | 29.09 | 1115 / 1118 |
stomach | 100% | 821.45 | 359 / 359 | 99% | 25.70 | 284 / 286 |
intestine | 100% | 1131.67 | 966 / 966 | 99% | 28.91 | 523 / 527 |
uterus | 100% | 1257.99 | 170 / 170 | 99% | 30.15 | 455 / 459 |
bladder | 100% | 1192.33 | 21 / 21 | 99% | 28.08 | 498 / 504 |
lung | 99% | 1003.40 | 571 / 578 | 100% | 30.69 | 1155 / 1155 |
thymus | 100% | 1078.78 | 653 / 653 | 99% | 22.32 | 596 / 605 |
prostate | 100% | 1086.43 | 245 / 245 | 98% | 22.67 | 494 / 502 |
kidney | 100% | 838.64 | 89 / 89 | 97% | 16.98 | 874 / 901 |
pancreas | 98% | 501.16 | 323 / 328 | 98% | 19.22 | 175 / 178 |
skin | 100% | 2026.88 | 1809 / 1809 | 94% | 23.78 | 443 / 472 |
adrenal gland | 100% | 1165.03 | 258 / 258 | 92% | 13.80 | 211 / 230 |
liver | 100% | 781.69 | 226 / 226 | 91% | 13.10 | 368 / 406 |
adipose | 100% | 1265.87 | 1204 / 1204 | 0% | 0 | 0 / 0 |
lymph node | 0% | 0 | 0 / 0 | 100% | 23.99 | 29 / 29 |
spleen | 100% | 1019.45 | 241 / 241 | 0% | 0 | 0 / 0 |
tonsil | 0% | 0 | 0 / 0 | 100% | 31.38 | 45 / 45 |
ureter | 0% | 0 | 0 / 0 | 100% | 9.66 | 1 / 1 |
blood vessel | 100% | 1064.49 | 1334 / 1335 | 0% | 0 | 0 / 0 |
muscle | 100% | 714.62 | 801 / 803 | 0% | 0 | 0 / 0 |
heart | 95% | 603.90 | 822 / 861 | 0% | 0 | 0 / 0 |
eye | 0% | 0 | 0 / 0 | 65% | 8.49 | 52 / 80 |
peripheral blood | 56% | 898.28 | 516 / 929 | 0% | 0 | 0 / 0 |
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_0006289 | Biological process | nucleotide-excision repair |
GO_0006366 | Biological process | transcription by RNA polymerase II |
GO_0006281 | Biological process | DNA repair |
GO_0006355 | Biological process | regulation of DNA-templated transcription |
GO_0097550 | Cellular component | transcription preinitiation complex |
GO_0000438 | Cellular component | core TFIIH complex portion of holo TFIIH complex |
GO_0005669 | Cellular component | transcription factor TFIID complex |
GO_0005654 | Cellular component | nucleoplasm |
GO_0000439 | Cellular component | transcription factor TFIIH core complex |
GO_0005675 | Cellular component | transcription factor TFIIH holo complex |
GO_0005634 | Cellular component | nucleus |
GO_0016251 | Molecular function | RNA polymerase II general transcription initiation factor activity |
GO_0005515 | Molecular function | protein binding |
GO_0046872 | Molecular function | metal ion binding |
Gene name | GTF2H3 |
Protein name | General transcription factor IIH subunit 3 (General transcription factor IIH polypeptide 3) General transcription factor IIH subunit 3 (Basic transcription factor 2 34 kDa subunit) (BTF2 p34) (General transcription factor IIH polypeptide 3) (TFIIH basal transcription factor complex p34 subunit) |
Synonyms | |
Description | FUNCTION: Component of the general transcription and DNA repair factor IIH (TFIIH) core complex, which is involved in general and transcription-coupled nucleotide excision repair (NER) of damaged DNA and, when complexed to CAK, in RNA transcription by RNA polymerase II. In NER, TFIIH acts by opening DNA around the lesion to allow the excision of the damaged oligonucleotide and its replacement by a new DNA fragment. In transcription, TFIIH has an essential role in transcription initiation. When the pre-initiation complex (PIC) has been established, TFIIH is required for promoter opening and promoter escape. Phosphorylation of the C-terminal tail (CTD) of the largest subunit of RNA polymerase II by the kinase module CAK controls the initiation of transcription. . FUNCTION: Component of the general transcription and DNA repair factor IIH (TFIIH) core complex, which is involved in general and transcription-coupled nucleotide excision repair (NER) of damaged DNA and, when complexed to CAK, in RNA transcription by RNA polymerase II. In NER, TFIIH acts by opening DNA around the lesion to allow the excision of the damaged oligonucleotide and its replacement by a new DNA fragment. In transcription, TFIIH has an essential role in transcription initiation. When the pre-initiation complex (PIC) has been established, TFIIH is required for promoter opening and promoter escape. Phosphorylation of the C-terminal tail (CTD) of the largest subunit of RNA polymerase II by the kinase module CAK controls the initiation of transcription. . FUNCTION: Component of the general transcription and DNA repair factor IIH (TFIIH) core complex, which is involved in general and transcription-coupled nucleotide excision repair (NER) of damaged DNA and, when complexed to CAK, in RNA transcription by RNA polymerase II. In NER, TFIIH acts by opening DNA around the lesion to allow the excision of the damaged oligonucleotide and its replacement by a new DNA fragment. In transcription, TFIIH has an essential role in transcription initiation. When the pre-initiation complex (PIC) has been established, TFIIH is required for promoter opening and promoter escape. Phosphorylation of the C-terminal tail (CTD) of the largest subunit of RNA polymerase II by the kinase module CAK controls the initiation of transcription. . FUNCTION: Component of the general transcription and DNA repair factor IIH (TFIIH) core complex, which is involved in general and transcription-coupled nucleotide excision repair (NER) of damaged DNA and, when complexed to CAK, in RNA transcription by RNA polymerase II. In NER, TFIIH acts by opening DNA around the lesion to allow the excision of the damaged oligonucleotide and its replacement by a new DNA fragment. In transcription, TFIIH has an essential role in transcription initiation. When the pre-initiation complex (PIC) has been established, TFIIH is required for promoter opening and promoter escape. Phosphorylation of the C-terminal tail (CTD) of the largest subunit of RNA polymerase II by the kinase module CAK controls the initiation of transcription. . FUNCTION: Component of the general transcription and DNA repair factor IIH (TFIIH) core complex, which is involved in general and transcription-coupled nucleotide excision repair (NER) of damaged DNA and, when complexed to CAK, in RNA transcription by RNA polymerase II. In NER, TFIIH acts by opening DNA around the lesion to allow the excision of the damaged oligonucleotide and its replacement by a new DNA fragment. In transcription, TFIIH has an essential role in transcription initiation. When the pre-initiation complex (PIC) has been established, TFIIH is required for promoter opening and promoter escape. Phosphorylation of the C-terminal tail (CTD) of the largest subunit of RNA polymerase II by the kinase module CAK controls the initiation of transcription. . FUNCTION: Component of the general transcription and DNA repair factor IIH (TFIIH) core complex, which is involved in general and transcription-coupled nucleotide excision repair (NER) of damaged DNA and, when complexed to CAK, in RNA transcription by RNA polymerase II. In NER, TFIIH acts by opening DNA around the lesion to allow the excision of the damaged oligonucleotide and its replacement by a new DNA fragment. In transcription, TFIIH has an essential role in transcription initiation. When the pre-initiation complex (PIC) has been established, TFIIH is required for promoter opening and promoter escape. Phosphorylation of the C-terminal tail (CTD) of the largest subunit of RNA polymerase II by the kinase module CAK controls the initiation of transcription. . FUNCTION: Component of the general transcription and DNA repair factor IIH (TFIIH) core complex, which is involved in general and transcription-coupled nucleotide excision repair (NER) of damaged DNA and, when complexed to CAK, in RNA transcription by RNA polymerase II. In NER, TFIIH acts by opening DNA around the lesion to allow the excision of the damaged oligonucleotide and its replacement by a new DNA fragment. In transcription, TFIIH has an essential role in transcription initiation. When the pre-initiation complex (PIC) has been established, TFIIH is required for promoter opening and promoter escape. Phosphorylation of the C-terminal tail (CTD) of the largest subunit of RNA polymerase II by the kinase module CAK controls the initiation of transcription. . FUNCTION: Component of the general transcription and DNA repair factor IIH (TFIIH) core complex, which is involved in general and transcription-coupled nucleotide excision repair (NER) of damaged DNA and, when complexed to CAK, in RNA transcription by RNA polymerase II. In NER, TFIIH acts by opening DNA around the lesion to allow the excision of the damaged oligonucleotide and its replacement by a new DNA fragment. In transcription, TFIIH has an essential role in transcription initiation. When the pre-initiation complex (PIC) has been established, TFIIH is required for promoter opening and promoter escape. Phosphorylation of the C-terminal tail (CTD) of the largest subunit of RNA polymerase II by the kinase module CAK controls the initiation of transcription. . FUNCTION: Component of the general transcription and DNA repair factor IIH (TFIIH) core complex, which is involved in general and transcription-coupled nucleotide excision repair (NER) of damaged DNA and, when complexed to CAK, in RNA transcription by RNA polymerase II. In NER, TFIIH acts by opening DNA around the lesion to allow the excision of the damaged oligonucleotide and its replacement by a new DNA fragment. In transcription, TFIIH has an essential role in transcription initiation. When the pre-initiation complex (PIC) has been established, TFIIH is required for promoter opening and promoter escape. Phosphorylation of the C-terminal tail (CTD) of the largest subunit of RNA polymerase II by the kinase module CAK controls the initiation of transcription. . |
Accessions | F5GX35 A0A087WYD5 Q13889 F5GXG6 ENST00000538533.5 ENST00000543341.7 [Q13889-1] ENST00000538845.5 ENST00000228955.11 [Q13889-2] F5H4K7 ENST00000618160.4 ENST00000536375.5 ENST00000543154.1 F5H3G1 F5H6X0 ENST00000542279.5 F5GWD3 ENST00000543415.5 H0YFF7 ENST00000539994.5 |