Last update 01 Nov 2024

PCDHB1

Last update 01 Nov 2024

Basic Info

Synonyms

PCDH-beta-1, PCDH-BETA1, PCDHB1

+ [2]

Introduction

Potential calcium-dependent cell-adhesion protein. May be involved in the establishment and maintenance of specific neuronal connections in the brain.

100 Clinical Results associated with PCDHB1

100 Translational Medicine associated with PCDHB1

0 Patents (Medical) associated with PCDHB1

Literatures (Medical) associated with PCDHB1

01 Jul 2015·Genes & NutritionQ3 · MEDICINE

Olfactory receptor genes cooperate with protocadherin genes in human extreme obesity

Q3 · MEDICINE

ArticleOA

Author: Freek G. Bouwman ; Marleen A. van Baak ; Radek Szklarczyk ; Ping Wang ; Erik E. J. G. Aller ; Edwin C. M. Mariman

Worldwide, the incidence of obesity has increased dramatically over the past decades. More knowledge about the complex etiology of obesity is needed in order to find additional approaches for treatment and prevention. Investigating the exome sequencing data of 30 extremely obese subjects (BMI 45-65 kg/m(2)) shows that predicted damaging missense variants in olfactory receptor genes on chromosome 1q and rare predicted damaging variants in the protocadherin (PCDH) beta-cluster genes on chromosome 5q31, reported in our previous work, co-localize in subjects with extreme obesity. This implies a synergistic effect between genetic variation in these gene clusters in the predisposition to extreme obesity. Evidence for a general involvement of the olfactory transduction pathway on itself could not be found. Bioinformatic analysis indicates a specific involvement of the PCDH beta-cluster genes in controlling tissue development. Further mechanistic insight needs to await the identification of the ligands of the 1q olfactory receptors. Eventually, this may provide the possibility to manipulate food flavor in a way to reduce the risk of overeating and of extreme obesity in genetically predisposed subjects.

01 Dec 2011·BMC NeuroscienceQ3 · MEDICINE

The protocadherins, PCDHB1 and PCDH7, are regulated by MeCP2 in neuronal cells and brain tissues: implication for pathogenesis of Rett syndrome

Q3 · MEDICINE

ArticleOA

Author: Sana Yokoi ; Takahiro Taira ; Kunio Miyake ; Takayuki Nakagawa ; Johji Inazawa ; Kazushi Endoh ; Yu-ichi Goto ; Takeo Kubota ; Masaki Soutome ; Kenichiro Takahashi ; Masayuki Itoh ; Takae Hirasawa ; Shinichi Kudo

BACKGROUNDRett syndrome is a neurodevelopmental and autistic disease caused by mutations of Methyl-CpG-binding protein 2 (MECP2) gene. MeCP2 protein is mainly expressed in neurons and binds to methylated gene promoters to suppress their expression, indicating that Rett syndrome is caused by the deregulation of target genes in neurons. However, it is likely that there are more unidentified neuronal MeCP2-targets associated with the neurological features of RTT.RESULTSUsing a genome-microarray approach, we found 22 genomic regions that contain sites potentially regulated by MeCP2 based on the features of MeCP2 binding, DNA methylation, and repressive histone modification in human cell lines. Within these regions, Chromatin immunoprecipitation (ChIP) analysis revealed that MeCP2 binds to the upstream regions of the protocadherin genes PCDHB1 and PCDH7 in human neuroblastoma SH-SY5Y cells. PCDHB1 and PCDH7 promoter activities were down-regulated by MeCP2, but not by MBD-deleted MeCP2. These gene expression were up-regulated following MeCP2 reduction with siRNA in SH-SY5Y cells and in the brains of Mecp2-null mice. Furthermore, PCDHB1 was up-regulated in postmortem brains from Rett syndrome patients.CONCLUSIONSWe identified MeCP2 target genes that encode neuronal adhesion molecules using ChIP-on-BAC array approach. Since these protocadherin genes are generally essential for brain development, aberrant regulation of these molecules may contribute to the pathogenesis of the neurological features observed in Rett syndrome.

PLoS ONEQ3 · CROSS-FIELD

Exome Sequencing Identifies Early Gastric Carcinoma as an Early Stage of Advanced Gastric Cancer

Q3 · CROSS-FIELD

ArticleOA

Author: Wang, Kai ; Lee, Jeeyun ; Kim, Seonwoo ; Park, Se Hoon ; Kang, Won Ki ; Bae, Jae Moon ; Kang, So Young ; Lee, Jun Ho ; Hwang, Woo Cheol ; Do, In-Gu ; Choi, Min-Gew ; Sohn, Tae Sung ; Jang, Jiryeon ; Kang, Guhyun ; Kim, Min Ji ; Park, Joon Oh ; Kim, Kyoung-Mee ; Park, Cheol Keun ; Kim, Sung

Gastric carcinoma is one of the major causes of cancer-related mortality worldwide. Early detection and treatment leads to an excellent prognosis in patients with early gastric cancer (EGC), whereas the prognosis of patients with advanced gastric cancer (AGC) remains poor. It is unclear whether EGCs and AGCs are distinct entities or whether EGCs are the beginning stages of AGCs. We performed whole exome sequencing of four samples from patients with EGC and compared the results with those from AGCs. In both EGCs and AGCs, a total of 268 genes were commonly mutated and independent mutations were additionally found in EGCs (516 genes) and AGCs (3104 genes). A higher frequency of C>G transitions was observed in intestinal-type compared to diffuse-type carcinomas (P = 0.010). The DYRK3, GPR116, MCM10, PCDH17, PCDHB1, RDH5 and UNC5C genes are recurrently mutated in EGCs and may be involved in early carcinogenesis.

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PCDHB1

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