SMC2

Last update 08 May 2025

Basic Info

Synonyms

CAP-E, CAPE, Chromosome-associated protein E

+ [8]

Introduction

Central component of the condensin complex, a complex required for conversion of interphase chromatin into mitotic-like condense chromosomes. The condensin complex probably introduces positive supercoils into relaxed DNA in the presence of type I topoisomerases and converts nicked DNA into positive knotted forms in the presence of type II topoisomerases.

100 Clinical Results associated with SMC2

100 Translational Medicine associated with SMC2

0 Patents (Medical) associated with SMC2

210

Literatures (Medical) associated with SMC2

01 Apr 2025·International Journal of Cancer

Search for germline gene variants in colorectal cancer families presenting with multiple primary colorectal cancers

Article

Author: Ambrozkiewicz, Filip ; Försti, Asta ; Hemminki, Kari ; Lubinski, Jan ; Marciniak, Magdalena

AbstractA double primary colorectal cancer (CRC) in a familial setting signals a high risk of CRC. In order to identify novel CRC susceptibility genes, we whole‐exome sequenced germline DNA from nine persons with a double primary CRC and a family history of CRC. The detected variants were processed by bioinformatics filtering and prioritization, including STRING protein–protein interaction and pathway analysis. A total of 150 missense, 19 stop‐gain, 22 frameshift and 13 canonical splice site variants fulfilled our filtering criteria. The STRING analysis identified 20 DNA repair/cell cycle proteins as the main cluster, related to genes CHEK2, EXO1, FAAP24, FANCI, MCPH1, POLL, PRC1, RECQL, RECQL5, RRM2, SHCBP1, SMC2, XRCC1, in addition to CDK18, ENDOV, ZW10 and the known mismatch repair genes. Another STRING network included extracellular matrix genes and TGFβ signaling genes. In the nine whole‐exome sequenced patients, eight harbored at least two candidate DNA repair/cell cycle/TGFβ signaling gene variants. The number of families is too small to provide evidence for individual variants but, considering the known role of DNA repair/cell cycle genes in CRC, the clustering of multiple deleterious variants in the present families suggests that these, perhaps jointly, contributed to CRC development in these families.

01 Mar 2025·Redox Biology

The antioxidant property of CAPE depends on TRPV1 channel activation in microvascular endothelial cells

Article

Author: Añazco, Carolina ; Zuñiga, Leandro ; Navarro, Carolina ; Hidalgo, Miltha ; Kreindl, Christine ; Railef, Bárbara ; Meneses-Pacheco, Jorge ; Rodríguez, Vania ; Soto-Alarcón, Sandra ; Porras, Omar ; Rubio, Vanessa

Caffeic acid phenethyl ester (CAPE) is a hydrophobic phytochemical typically found in propolis that acts as an antioxidant, anti-inflammatory and cardiovascular protector, among several other properties. However, the molecular entity responsible for recognising CAPE is unknown, and whether that molecular interaction is involved in developing an antioxidant response in the target cells remains an unanswered question. Herein, we hypothesized that a subfamily of TRP ion channels works as the molecular entity that recognizes CAPE at the plasma membrane and allows a fast shift in the antioxidant capacity of intact endothelial cells (EC). By monitoring cytoplasmic Ca²⁺ in a microvascular EC model, we compared the calcium responses evoked by three structurally related compounds: caffeic acid phenethyl ester, neochlorogenic acid and caffeic acid. Only CAPE induced rapid and transient calcium responses at nanomolar concentrations together with a gradual increase in cytoplasmic sodium levels, suggesting the activation of a non-selective cationic permeation at the plasma membrane. Electrophysiological as well as pharmacological, and RNA silencing assays confirmed the involvement of TRPV1 in the recognition of CAPE by ECs. Finally, we demonstrated that Ca²⁺ influx by TRPV1 was necessary for recording CAPE-induced cytoplasmic redox changes, a phenomenon captured in real-time in ECs expressing the HyPer biosensor. Our data depict a molecular mechanism behind the antioxidant effect of CAPE in endothelial cells, connecting the activation of TRPV1 ion channels, cytoplasmic calcium increase, and a reduction of disulfide bonds on a redox biosensor. This phenomenon occurs within seconds to minutes and contributes to a better understanding of the mechanisms underlying the vasodilatory effect of CAPE and other compounds that interact with TRPV1 in the vascular bed.

01 Mar 2025·Journal of Cellular Physiology

SMC2 and Condensin II Subunits Are Essential for the Development of Hematopoietic Stem and Progenitor Cells in Zebrafish

Article

Author: Nam, Uijeong ; Lee, Yoonsung ; Myung, Kyungjae ; Choi, Eun Young ; Ko, Hwa Soo ; Choi, Taesoo ; Ahn, Soyul ; Ra, Jae Sun ; Shin, Unbeom ; Kang, Ji Wan ; Kim, Yun Hak ; Oh, Chang‐Kyu ; Yu, Sanghyeon ; Kim, Man S.

ABSTRACTHematopoietic stem and progenitor cells (HSPCs) play a pivotal role in blood cell production, maintaining the health and homeostasis of individuals. Dysregulation of HSPC function can lead to blood‐related diseases, including cancer. Despite its importance, our understanding of the genes and pathways underlying HSPC development and the associated pathological mechanisms remains limited. To elucidate these unknown mechanisms, we analyzed databases of patients with blood disorders and performed functional gene studies using zebrafish. We employed bioinformatics tools to explore three public databases focusing on patients with myelodysplastic syndrome (MDS) and related model studies. This analysis identified significant alterations in several genes, especially SMC2 and other condensin‐related genes, in patients with MDS. To further investigate the role of Smc2 in hematopoiesis, we generated smc2 loss‐of‐function zebrafish mutants using CRISPR mutagenesis. Further analyses of the mutants revealed that smc2 depletion induced G2/M cell cycle arrest in HSPCs, leading to their maintenance and expansion failure. Notably, although the condensin II subunits (ncaph2, ncapg2, and ncapd3) were essential for HSPC maintenance, the condensin I subunits did not affect HSPC development. These findings emphasize the crucial role of condensin II in ensuring healthy hematopoiesis via promoting HSPC proliferation.

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SMC2

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