Basic Information
Gene Structure
upstream:
Get Sequence
Domain
| Database | EntryID | E-Value | Start | end | InterPro ID | Description |
|---|
Regulation&Interaction
Annotation
Orthologous Group
| Orthologous ID | Species Number | All hits in PereRegDB | Hits of this species | Orthologous Detail |
|---|
Expression Profile
| DataSet | Number of Samples expressed(TPM>1) | Mean | Min | Max | Standard deviation(SD) | Coeffcient variation(CV) |
|---|
Pathway
| GO Term | Description | GO Category |
|---|---|---|
| GO:0003674 | molecular_function | MF |
| GO:0003700 | DNA-binding transcription factor activity | MF |
| GO:0005575 | cellular_component | CC |
| GO:0005622 | intracellular anatomical structure | CC |
| GO:0005623 | obsolete cell | CC |
| GO:0005634 | nucleus | CC |
| GO:0006355 | regulation of DNA-templated transcription | BP |
| GO:0008150 | biological_process | BP |
| GO:0009889 | regulation of biosynthetic process | BP |
| GO:0010033 | response to organic substance | BP |
| GO:0010200 | response to chitin | BP |
| GO:0010243 | response to organonitrogen compound | BP |
| GO:0010468 | regulation of gene expression | BP |
| GO:0010556 | regulation of macromolecule biosynthetic process | BP |
| GO:0019219 | regulation of nucleobase-containing compound metabolic process | BP |
| GO:0019222 | regulation of metabolic process | BP |
| GO:0031323 | regulation of cellular metabolic process | BP |
| GO:0031326 | regulation of cellular biosynthetic process | BP |
| GO:0042221 | response to chemical | BP |
| GO:0042493 | response to xenobiotic stimulus | BP |
| GO:0043226 | organelle | CC |
| GO:0043227 | membrane-bounded organelle | CC |
| GO:0043229 | intracellular organelle | CC |
| GO:0043231 | intracellular membrane-bounded organelle | CC |
| GO:0044424 | obsolete intracellular part | CC |
| GO:0044464 | obsolete cell part | CC |
| GO:0050789 | regulation of biological process | BP |
| GO:0050794 | regulation of cellular process | BP |
| GO:0050896 | response to stimulus | BP |
| GO:0051171 | regulation of nitrogen compound metabolic process | BP |
| GO:0051252 | regulation of RNA metabolic process | BP |
| GO:0060255 | regulation of macromolecule metabolic process | BP |
| GO:0065007 | biological regulation | BP |
| GO:0080090 | regulation of primary metabolic process | BP |
| GO:0140110 | transcription regulator activity | MF |
| GO:1901698 | response to nitrogen compound | BP |
| GO:1901700 | response to oxygen-containing compound | BP |
| GO:1903506 | regulation of nucleic acid-templated transcription | BP |
| GO:2000112 | regulation of cellular macromolecule biosynthetic process | BP |
| GO:2001141 | regulation of RNA biosynthetic process | BP |
| KEGG Term | Name | Description |
|---|---|---|
| map04626 | Plant-pathogen interaction | Plants lack animal-like adaptive immunity mechanisms, and therefore have evolved a specific system with multiple layers against invading pathogens. The primary response includes the perception of pathogens by cell-surface pattern-recognition receptors (PRRs) and is referred to as PAMP-triggered immunity (PTI). Activation of FLS2 and EFR triggers MAPK signaling pathway that activates defense genes for antimictobial compounds. The increase in the cytosolic Ca2+ concentration is also a regulator for production of reactive oxygen species and localized programmed cell death/hypersensitive response. The secondary response is called effector-triggered immunity (ETI). Pathogens can acquire the ability to suppress PTI by directly injecting effector proteins into the plant cell through secretion systems. In addition, pathogens can manipulate plant hormone signaling pathways to evade host immune responses using coronatine toxin. Some plants possess specific intracellular surveillance proteins (R proteins) to monitor the presence of pathogen virulence proteins. This ETI occurs with localized programmed cell death to arrest pathogen growth, resulting in cultivar-specific disease resistance. |
| map04626 | Plant-pathogen interaction | Plants lack animal-like adaptive immunity mechanisms, and therefore have evolved a specific system with multiple layers against invading pathogens. The primary response includes the perception of pathogens by cell-surface pattern-recognition receptors (PRRs) and is referred to as PAMP-triggered immunity (PTI). Activation of FLS2 and EFR triggers MAPK signaling pathway that activates defense genes for antimictobial compounds. The increase in the cytosolic Ca2+ concentration is also a regulator for production of reactive oxygen species and localized programmed cell death/hypersensitive response. The secondary response is called effector-triggered immunity (ETI). Pathogens can acquire the ability to suppress PTI by directly injecting effector proteins into the plant cell through secretion systems. In addition, pathogens can manipulate plant hormone signaling pathways to evade host immune responses using coronatine toxin. Some plants possess specific intracellular surveillance proteins (R proteins) to monitor the presence of pathogen virulence proteins. This ETI occurs with localized programmed cell death to arrest pathogen growth, resulting in cultivar-specific disease resistance. |