SMC4 Antibodies

Structural maintenance of chromosomes protein 4 (SMC4)

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.

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Gene Information

Human
Gene Name:	SMC4
Uniprot:	Q9NTJ3
Entrez:	10051

Family

Belongs to:
SMC family

Alternative Names

CAP-C; CAPCSMC4 structural maintenance of chromosomes 4-like 1 (yeast); Chromosome-associated polypeptide C; hCAP-CSMC4 (structural maintenance of chromosomes 4, yeast)-like 1; SMC protein 4; SMC4 structural maintenance of chromosomes 4-like 1; SMC-4; SMC4L1; structural maintenance of chromosomes 4; structural maintenance of chromosomes protein 4; XCAP-C homolog

Molecular Weight

Mass (kDA):
147.182 kDA

Genomic Context

Human
Location:	3q25.33
Sequence:	3; NC_000003.12 (160399638..160434953)

Tissue Specificity

Widely expressed. Higher expression in testis, colon, thymus.

Subcellular Localizations

Nucleus. Cytoplasm. Chromosome. In interphase cells, the majority of the condensin complex is found in the cytoplasm, while a minority of the complex is associated with chromatin. A subpopulation of the complex however remains associated with chromosome foci in interphase cells. During mitosis, most of the condensin complex is associated with the chromatin. At the onset of prophase, the regulatory subunits of the complex are phosphorylated by CDC2, leading to condensin's association with chromosome arms and to chromosome condensation. Dissociation from chromosomes is observed in late telophase

Diseases

• Neoplasms
• Cell Transformation, Neoplastic
• Malignant Neoplasms
• Mammary Neoplasms
• Cell Invasion
• Mitochondrial Dna Depletion
• Liver Carcinoma
• Malignant Neoplasm Of Breast
• Glioma
• Malignant Paraganglionic Neoplasm
• Malignant Neoplasm Of Liver
• Malignant Glioma

• Brain Neoplasms
• Neoplasm Invasiveness
• Carcinoma
• Dental Fluorosis, Acquired
• Karyomegaly
• Chromosome Breakage
• Chimera Disorder

Interacting Proteins

• NCAPH
• NCAPH2
• SMC2

Pathways

• Chromosome Condensation
• Mitosis
• Dna Repair
• Metaphase
• Cell Cycle
• Sister Chromatid Cohesion
• Interphase
• Chromosome Segregation
• Cell Division
• Localization
• Mitotic Chromosome Condensation
• Dosage Compensation
• Dna Recombination

• Regulation Of Gene Expression
• Anaphase
• Meiosis
• Cell Proliferation
• Dna Replication
• S Phase
• Chromosome Organization

PTMs

• Phosphorylation

• Cleavage

• Dephosphorylation

Research Areas

• Cell Cycle and Replication
• Core ESC-Like Genes
• DNA Repair
• Stem Cell Markers

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/SMC4

Best Uses Of The SMC4 Marker

Antibodies to SMC4 are used in many biological assays to detect SMC4. These antibodies can be either polyclonal or monoclonal. They react with the protein in several samples from different species. Boster Bio uses rabbit and mouse for the development of their antibodies to SMC4. SMC4 is a protein that functions in the conversion of interphase chromatin into mitotic-like condensed chromosomes, and in the presence of type II topoisomerases, it converts nicked DNA to positive knotted forms.

SMC2 functions in early embryonic development

The function of SMC2 in early embryonic development is unknown, but its expression in postembryonic cells is required for chromosome segregation. Defective progeny display aneuploid nuclei and irregular chromatin structure. The phenotypes of smc-4(RNAi) and mix-1(RNAi) embryos are similar. Here, we review some of the findings.

ESCs are known to be able to maintain genome integrity by coping with chromosomal aberrations and replication stresses. They also undergo cell proliferation and differentiation. Knockdown of SMC2 inhibits the initiation of cell differentiation and increases the intensity of RB and CAP-D3 signals in metaphase. These results show the importance of SMC2 during early embryonic development.

The effects of SMC2 knockdown on embryo development are complex and diverse. Knockdown of CLTC causes failures in metaphase plate formation. In addition to affecting zygotic to embryo transition, CLTC impairs the formation of later embryos. The denominator for percent of embryo development was the number of MII stage oocytes. Disrupting SMC2 function before the two-cell stage results in significant reduction in the number of two-cell, four-cell, eight-cell, and morula embryos.

SMC2 recruits the overexpressed genes CLTC in hepatocellular carcinoma and colonic tumors. It also forms an inter-MT bridge and stabilizes kinetochore fibers. However, its function in early embryonic development remains largely unknown. Further studies are required to determine if the protein localizes differently in mice and sheep. But, for now, this molecule is a major player in the process of mitotic spindle assembly.

Molecular analyses have shown that SMC2 has multiple roles in embryonic development. Its function has been suggested by a recent study in sheep and mouse oocytes. It also helps the oocytes to undergo meiotic maturation. This process involves the development of oocytes, resulting in the development of embryonic organs. In addition, SMC2 can also regulate the development of the limbs and the heart.

Furthermore, CLTC is an important factor during the meiotic process in sheep oocytes. It regulates spindle dynamics and plays a crucial role during early embryonic development. Furthermore, CLTC is involved in regulating chromosome separation in ESCs. The role of CLTC is unclear, but it has been shown to be essential for early embryonic development. If the gene SMC2 is expressed in sheep oocytes, the mice will have more ectopically expressed REC8.

It is responsible for liver expansion

The liver's morphogenesis is divided into two phases: the budding and growth phases. Between 24 and 50 hpf, the liver undergoes dramatic changes in size, shape, and placement. At 48 hpf, the liver begins to expand. Loss of the SMC4 marker did not affect the specification of hepatoblasts. Furthermore, loss of SMC2 did not affect the expression of early endodermal or hepatoblast markers.

In addition, SMC2 and SMC4 had essential roles in liver expansion. In both WT and SMC2-/ larvae, a high proportion of dividing cells was observed. However, in the SMC2-/ mutants, the liver cell proliferation rate was reduced. Furthermore, TUNEL assays performed on liver region of zebrafish larvae at 96 hpf showed active apoptosis in liver cells. However, in WT larvae, no apoptotic cells were detected.

In addition, studies have revealed that SMC2 is required for the development of the digestive system in zebrafish. Further, zebrafish also require the SMC2 gene, which is required for the formation of the liver. In this way, both genes play essential roles in the liver's development. However, in humans, SMC2 is essential for liver expansion. But despite its importance in liver development, its function is still unknown.

In addition, the SMC2-/ mutants show extensive apoptosis. The loss of p53 inhibits hepatocyte apoptosis, a key pathway of the apoptotic cascade. The loss of p53 may rescue the SMC2-/ mutant liver phenotype. Alternatively, loss of SMC2 and p53 may lead to apoptosis.

The SMC2 gene is also associated with the development of multiple organs in zebrafish. In human embryogenesis, it is implicated in the development of multiple organs. Furthermore, the SMC2 gene is important in the formation of multiple organs during embryogenesis. The SMC2 gene is essential for liver expansion and function. Further studies are needed to determine if SMC4 is indeed involved in liver expansion.

It causes mild abnormal phenotypes in SMC2-/- early developing embryos

The human gene SMC2 is responsible for the development of the central nervous system. Early developmental embryos with mutant SMC2 show smaller heads and eyes, and die by 7 days of age. The gene is expressed in all cells of the developing embryo, but its expression is not increased in the late stage of development. This may be due to the redundant function of SMC4.

In zebrafish, SMC2 has an important role during liver morphogenesis. When the gene is knocked out, the embryos develop with reduced liver size. SMC2-/ embryos express more apoptotic pathways, which contribute to cell death. The role of p53-dependent apoptotic signaling in the formation of the small liver is unclear, but it partially rescues the liver size in SMC2-/ embryos.

Although SMC2 has a central role in chromosome organization and segregation, its function in embryonic development is not fully understood. Its homozygous state results in lethal embryos, and depletion of the gene leads to a small liver phenotype in SMC2-/ mice. The gene was also deleted using a CRISPR/Cas9-dependent gene knockout approach.

The genes responsible for these phenotypes have been identified by using fluorescent microscope. Inbred fish were used to generate (SMC2-/-; p53-/-) mutants. The resulting embryos were identified using dsRed fluorescence. In addition to dsRed fluorescence, tail-PCR was performed on 96-hpf embryos to determine genotype.

Loss of SMC2 in early developing embryos results in blockages of cell cycles in the M-phase. This leads to defects in chromosome segregation. Consequently, SMC2-/ embryos have smaller livers than WT embryos. In addition, liver size in SMC2-/ embryos is reduced by more than half compared to WT embryos.

Mutations in Smc proteins are associated with chromosomal abnormalities, but their function is still unknown. In fruit flies, Smc5/6 function was studied. Loss of Smc5/6 caused an arrest in embryo development and considerable delay in embryonic development. It was also associated with increased anaphase-bridge formation. However, these findings require further investigation.

It is unknown whether the absence of SMC2 leads to a lethal phenotype in early development. Loss of the gene does not affect liver bud expression in the early stages of development, although it inhibits the expansion of the liver bud. However, the loss of SMC2 causes an increased amount of g-H2AX foci in the liver.