MLLT3: Key Regulator of Mitochondrial Fusion and Diseases (G4300)

Target Name: MLLT3

NCBI ID: G4300

MLLT3

Other Name(s): MLLT3 variant 1 | Myeloid/lymphoid or mixed-lineage leukemia translocated to chromosome 3 protein | YEATS domain-containing protein 3 | MLLT3 super elongation complex subunit | MLLT3 super elongation complex subunit, transcript variant 1 | Protein AF-9 (isoform a) | FLJ2035 | AF9_HUMAN | Myeloid/lymphoid or mixed-lineage leukemia (trithorax (Drosophila) homolog); translocated to chromosome 3 | myeloid/lymphoid or mixed-lineage leukemia (trithorax homolog); translocated to, 3 | myeloid/lymphoid or mixed-lineage leukemia (trithorax homolog, Drosophila); translocated to, 3 | KMT2A/MLLT3 fusion protein | myeloid/lymphoid or mixed-lineage leukemia; translocated to 3 | OTTHUMP00000045120 | Protein AF-9 | YEATS3 | AF9 | ALL1-fused gene from chromosome 9 protein | myeloid/lymphoid or mixed-lineage leukemia translocated to chromosome 3 protein

MLLT3: Key Regulator of Mitochondrial Fusion and Diseases

MLLT3 (MLLT3 variant 1) is a protein that is expressed in various tissues of the body, including the brain, heart, and skeletal muscles. It is a key regulator of mitochondrial fusion and has been implicated in a number of diseases, including neurodegenerative disorders, cardiomyopathy, and cancer.

MLLT3 is a member of the MLLT family of proteins, which are known for their role in regulating mitochondrial fusion and dynamics. MLLT1 and MLLT2 are also known as the MLLT1-2 complex, and MLLT3 is the third member of the family. The MLLT3 protein is a 21 kDa protein that is expressed in various tissues of the body, including the brain, heart, and skeletal muscles.

One of the key functions of MLLT3 is its role in regulating mitochondrial fusion. Mitochondrial fusion is the process by which two mitochondria fuse to form a single mitochondria, a process that is critical for energy production. MLLT3 is involved in regulating the fusion of mitochondria from the cytoplasm to the mitochondrial membrane.

MLLT3 has also been shown to be involved in a number of other cellular processes, including cell signaling, DNA replication, and apoptosis (programmed cell death). It is a negative regulator of the PI3K/Akt signaling pathway, which is a pathway that is involved in a variety of cellular processes, including cell survival, growth, and angiogenesis (the formation of new blood vessels).

In addition to its role in regulating mitochondrial fusion, MLLT3 has also been shown to be involved in the regulation of a variety of cellular processes, including cell signaling, DNA replication, and apoptosis. It is a negative regulator of the PI3K/Akt signaling pathway, which is a pathway that is involved in a variety of cellular processes, including cell survival, growth, and angiogenesis.

MLLT3 is also associated with a number of diseases, including neurodegenerative disorders, cardiomyopathy, and cancer. For example, studies have shown that MLLT3 is overexpressed in the brains of individuals with neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease. Similarly, MLLT3 has also been shown to be overexpressed in the hearts of individuals with cardiomyopathy, a condition in which the heart muscle becomes weakened or does not function properly.

In addition to its association with neurodegenerative disorders and cardiomyopathy, MLLT3 is also thought to be involved in the regulation of a variety of cellular processes that are critical for human health. For example, studies have shown that MLLT3 is involved in the regulation of cell apoptosis, which is the process by which cells are programmed to die. MLLT3 has been shown to play a negative role in the regulation of cell apoptosis, which may have implications for the treatment of a variety of diseases.

In conclusion, MLLT3 is a protein that is involved in a variety of cellular processes that are critical for human health. Its role in regulating mitochondrial fusion and its association with the regulation of cell apoptosis make it an attractive target for drug development. Further research is needed to fully understand the role of MLLT3 in human health and to develop effective treatments for a variety of diseases.

Protein Name: MLLT3 Super Elongation Complex Subunit

Functions: Chromatin reader component of the super elongation complex (SEC), a complex required to increase the catalytic rate of RNA polymerase II transcription by suppressing transient pausing by the polymerase at multiple sites along the DNA (PubMed:20159561, PubMed:20471948, PubMed:25417107, PubMed:27105114, PubMed:27545619). Specifically recognizes and binds acylated histone H3, with a preference for histone H3 that is crotonylated (PubMed:25417107, PubMed:27105114, PubMed:27545619, PubMed:30374167, PubMed:30385749). Crotonylation marks active promoters and enhancers and confers resistance to transcriptional repressors (PubMed:25417107, PubMed:27105114, PubMed:27545619). Recognizes and binds histone H3 crotonylated at 'Lys-9' (H3K9cr), and with slightly lower affinity histone H3 crotonylated at 'Lys-18' (H3K18cr) (PubMed:27105114). Also recognizes and binds histone H3 acetylated and butyrylated at 'Lys-9' (H3K9ac and H3K9bu, respectively), but with lower affinity than crotonylated histone H3 (PubMed:25417107, PubMed:27105114, PubMed:30385749). In the SEC complex, MLLT3 is required to recruit the complex to crotonylated histones (PubMed:27105114, PubMed:27545619). Recruitment of the SEC complex to crotonylated histones promotes recruitment of DOT1L on active chromatin to deposit histone H3 'Lys-79' methylation (H3K79me) (PubMed:25417107). Plays a key role in hematopoietic stem cell (HSC) maintenance by preserving, rather than confering, HSC stemness (PubMed:31776511). Acts by binding to the transcription start site of active genes in HSCs and sustaining level of H3K79me2, probably by recruiting DOT1L (PubMed:31776511)

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•   expression level;
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The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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