General Information of the Molecule (ID: Mol00244)
Name
Transcription regulator protein BACH2 (BACH2) ,Homo sapiens
Synonyms
BTB and CNC homolog 2
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Molecule Type
Protein
Gene Name
BACH2
Gene ID
60468
Location
chr6:89926528-90296843[-]
Sequence
MSVDEKPDSPMYVYESTVHCTNILLGLNDQRKKDILCDVTLIVERKEFRAHRAVLAACSE
YFWQALVGQTKNDLVVSLPEEVTARGFGPLLQFAYTAKLLLSRENIREVIRCAEFLRMHN
LEDSCFSFLQTQLLNSEDGLFVCRKDAACQRPHEDCENSAGEEEDEEEETMDSETAKMAC
PRDQMLPEPISFEAAAIPVAEKEEALLPEPDVPTDTKESSEKDALTQYPRYKKYQLACTK
NVYNASSHSTSGFASTFREDNSSNSLKPGLARGQIKSEPPSEENEEESITLCLSGDEPDA
KDRAGDVEMDRKQPSPAPTPTAPAGAACLERSRSVASPSCLRSLFSITKSVELSGLPSTS
QQHFARSPACPFDKGITQGDLKTDYTPFTGNYGQPHVGQKEVSNFTMGSPLRGPGLEALC
KQEGELDRRSVIFSSSACDQVSTSVHSYSGVSSLDKDLSEPVPKGLWVGAGQSLPSSQAY
SHGGLMADHLPGRMRPNTSCPVPIKVCPRSPPLETRTRTSSSCSSYSYAEDGSGGSPCSL
PLCEFSSSPCSQGARFLATEHQEPGLMGDGMYNQVRPQIKCEQSYGTNSSDESGSFSEAD
SESCPVQDRGQEVKLPFPVDQITDLPRNDFQMMIKMHKLTSEQLEFIHDVRRRSKNRIAA
QRCRKRKLDCIQNLECEIRKLVCEKEKLLSERNQLKACMGELLDNFSCLSQEVCRDIQSP
EQIQALHRYCPVLRPMDLPTASSINPAPLGAEQNIAASQCAVGENVPCCLEPGAAPPGPP
WAPSNTSENCTSGRRLEGTDPGTFSERGPPLEPRSQTVTVDFCQEMTDKCTTDEQPRKDY
T
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Function
Transcriptional regulator that acts as repressor or activator. Binds to Maf recognition elements (MARE). Plays an important role in coordinating transcription activation and repression by MAFK. Induces apoptosis in response to oxidative stress through repression of the antiapoptotic factor HMOX1. Positively regulates the nuclear import of actin. Is a key regulator of adaptive immunity, crucial for the maintenance of regulatory T-cell function and B-cell maturation.
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Uniprot ID
BACH2_HUMAN
Ensembl ID
ENSG00000112182
HGNC ID
HGNC:14078
        Click to Show/Hide the Complete Species Lineage
Kingdom: Metazoa
Phylum: Chordata
Class: Mammalia
Order: Primates
Family: Hominidae
Genus: Homo
Species: Homo sapiens
Type(s) of Resistant Mechanism of This Molecule
  UAPP: Unusual Activation of Pro-survival Pathway
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
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Docetaxel
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Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Unusual Activation of Pro-survival Pathway (UAPP) Click to Show/Hide
Disease Class: Prostate cancer [1]
Sensitive Disease Prostate cancer [ICD-11: 2C82.0]
Sensitive Drug Docetaxel
Molecule Alteration Expression
Up-regulation
Experimental Note Identified from the Human Clinical Data
Cell Pathway Regulation miR193a-5p/Bach2/HO1 signaling pathway Inhibition hsa05206
In Vitro Model DU-145 cells Prostate Homo sapiens (Human) CVCL_0105
LNCaP cells Prostate Homo sapiens (Human) CVCL_0395
PC3 cells Prostate Homo sapiens (Human) CVCL_0035
T24 cells Bladder Homo sapiens (Human) CVCL_0554
RWPE-1 cells Prostate Homo sapiens (Human) CVCL_3791
UM-UC-3 cells Bladder Homo sapiens (Human) CVCL_1783
In Vivo Model Nude mouse xenograft model Mus musculus
Experiment for
Molecule Alteration
Western blot analysis; Luciferase reporter assay; Immunofluorescence staining assay
Experiment for
Drug Resistance
TUNEL assays
Mechanism Description Silencing of miR193a-5p or blockade of the miR193a-5p-Bach2-HO-1 pathway enhances sensitization of PC3 cells to docetaxel-induced apoptosis. Docetaxel-induced miR193a-5p upregulation, which in turn inhibits Bach2 expression and thus relieves Bach2 repression of HO-1 expression, partly counteracted docetaxel-induced apoptosis.
Disease- and Tissue-specific Abundances of This Molecule
ICD Disease Classification 02
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Prostate cancer [ICD-11: 2C82]
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Differential expression of molecule in resistant diseases
The Studied Tissue Prostate
The Specified Disease Prostate cancer
The Expression Level of Disease Section Compare with the Healthy Individual Tissue p-value: 1.08E-01; Fold-change: -1.96E-01; Z-score: -2.73E-01
Molecule expression in the diseased tissue of patients
Molecule expression in the normal tissue of healthy individuals
Disease-specific Molecule Abundances Click to View the Clearer Original Diagram
Tissue-specific Molecule Abundances in Healthy Individuals
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References
Ref 1 Silencing of miR-193a-5p increases the chemosensitivity of prostate cancer cells to docetaxel. J Exp Clin Cancer Res. 2017 Dec 8;36(1):178. doi: 10.1186/s13046-017-0649-3.

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