Last update 01 Nov 2024

PAX2

Last update 01 Nov 2024

Basic Info

Synonyms

paired box 2, Paired box protein Pax-2, PAX-2

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Introduction

Transcription factor that may have a role in kidney cell differentiation (PubMed:24676634). Has a critical role in the development of the urogenital tract, the eyes, and the CNS.

Drugs associated with PAX2

Targeting PAX2 (Phigenix)

Target

PAX2

Mechanism

PAX2 modulators

Active Org.

Phigenix, Inc.

Originator Org.

Phigenix, Inc.

Active Indication

Breast Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CN115724966

Patent Mining

Target

PAX2

Mechanism-

Active Org.

Beijing Zhongshan Golden Bridge Biotechnology Co. Ltd.

Originator Org.

Beijing Zhongshan Golden Bridge Biotechnology Co. Ltd.

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with PAX2

100 Translational Medicine associated with PAX2

0 Patents (Medical) associated with PAX2

1,507

Literatures (Medical) associated with PAX2

01 Jan 2025·Developmental Biology

Pax2a, Pax5 and Cdh1-β-catenin, but not Wnt, protect sensory hair cells from destabilizing effects of fgf signaling on cell adhesion

Article

Author: Roberson, Whitney ; Holland, Jorden N. ; Holland, Jorden N ; Riley, Bruce B ; Riley, Bruce B.

During inner ear development, specification of sensory epithelia requires dynamic regulation of Fgf signaling. In zebrafish, high levels of Fgf are necessary and sufficient to specify the utricular/vestibular macula, whereas the saccular/auditory macula requires a discreet lower level of Fgf. Transcription factors Pax2a and Pax5 act downstream of Fgf to help specify utricular identity, loss of which leads to sporadic extrusion of hair cells from the utricular macula. The mechanism for utricular instability is not clear but is potentially related to reduced expression of cdh1/Ecad caused by disruption of pax2a. Here we find that utricular hair cells in pax2-/- and pax5-/- mutants gradually lose adhesive contact with the macula, leading to ejection of intact hair cells from either the basal or apical surface. The phenotype is far more severe in pax2a-/- mutants and is progressive, resulting in loss of large swaths of the utricular hair cells by 82 hpf. Instability is caused by elevated Fgf signaling in the utricle, as modest reduction of Fgf signaling with a low dose of SU5402 prevents hair cell loss in pax2a-/- mutants. Misexpression of cdh1/Ecad in pax2a-/- mutants partially rescues pax2a-/- mutants. Elevating β-catenin levels by treatment with BIO, or misexpression of a mutant form of β-catenin lacking transcriptional activity but retaining cell adhesion function, fully rescues pax2a-/- mutants. In contrast, Wnt signaling is not required for utricular stability. Thus, Pax2/5 factors serve to counteract the destabilizing effects of elevated Fgf signaling needed to specify utricular identity.

01 Nov 2024·Histopathology

Retained PAX2 expression associated with DNA mismatch repair deficiency in endometrial endometrioid adenocarcinoma

Article

Author: Yang, Bin ; X. Zhang, Gloria

AimsLoss of expression of tumour suppressor PAX2 and MMR deficiency (dMMR) has been frequently seen in endometrial endometrioid adenocarcinoma (EEC). However, the relationship between PAX2 expression and MMR status is unknown.Methods and ResultsWe studied the PAX2 expression and examined its association with MMR status at the protein and genetic levels in 180 cases of EEC. Overall, total loss of PAX2 expression was found in about 70%, while retained PAX2 expression was seen in 30% of EEC. Among 125 cases with loss of PAX2, 68.8% were found in EECs with pMMR, while 31.2% were seen in those with dMMR. Among 55 cases of EECs with retained PAX2 expression, 92.7% were EECs with dMMR and 7.3% were those with pMMR (P < 0.001). While dMMR cases with MLH1 hypermethylation show almost equal retained or loss of PAX2 expression (52% versus 48%), dMMR with genetic alterations had significantly more retained PAX2 expression than loss of PAX2 (92.3% versus 7.7%), regardless of somatic or germline mutations. Loss of PAX2 was observed in 97.3% of dMMR with MLH1 hypermethylation compared to 2.7% of dMMR with genetic alterations (P < 0.001). Aggressive features such as higher tumour grades (FIGO 2–3) and advanced clinical stage (T2–T4) were significantly more frequently seen in dMMR with retained PAX2 expression, compared those to pMMR with loss of PAX2 expression.ConclusionOur study demonstrates a close correlation between retained PAX2 expression and dMMR in EEC. The molecular mechanism and clinical significance linking these two pathways in EEC remains to be unravelled.

01 Sep 2024·Cells & Development

The Oct4-related PouV gene, pou5f3, mediates isthmus development in zebrafish by directly and dynamically regulating pax2a

Article

Author: Takemoto, Kazumasa ; Isobe, Daiki ; Dobashi, Yurie ; Miura, Yuhei ; Yamasu, Kyo ; Saito, Shinji ; Maekawa, Masato

Using a transgenic zebrafish line harboring a heat-inducible dominant-interference pou5f3 gene (en-pou5f3), we reported that this PouV gene is involved in isthmus development at the midbrain-hindbrain boundary (MHB), which patterns the midbrain and cerebellum. Importantly, the functions of pou5f3 reportedly differ before and after the end of gastrulation. In the present study, we examined in detail the effects of en-pou5f3 induction on isthmus development during embryogenesis. When en-pou5f3 was induced around the end of gastrulation (bud stage), the isthmus was abrogated or deformed by the end of somitogenesis (24 hours post-fertilization). At this stage, the expression of MHB markers -- such as pax2a, fgf8a, wnt1, and gbx2 -- was absent in embryos lacking the isthmus structure, whereas it was present, although severely distorted, in embryos with a deformed isthmus. We further found that, after en-pou5f3 induction at late gastrulation, pax2a, fgf8a, and wnt1 were immediately and irreversibly downregulated, whereas the expression of en2a and gbx2 was reduced only weakly and slowly. Induction of en-pou5f3 at early somite stages also immediately downregulated MHB genes, particularly pax2a, but their expression was restored later. Overall, the data suggested that pou5f3 directly upregulates at least pax2a and possibly fgf8a and wnt1, which function in parallel in establishing the MHB, and that the role of pou5f3 dynamically changes around the end of gastrulation. We next examined the transcriptional regulation of pax2a using both in vitro and in vivo reporter analyses; the results showed that two upstream 1.0-kb regions with sequences conserved among vertebrates specifically drove transcription at the MHB. These reporter analyses confirmed that development of the isthmic organizer is regulated by PouV through direct regulation of pax2/pax2a in vertebrate embryos.

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PAX2

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