MAP1S

Official Full Name

microtubule associated protein 1S

Organism

Homo sapiens

GeneID

55201

Background

Enables DNA binding activity and cytoskeletal protein binding activity. Involved in metaphase chromosome alignment; microtubule cytoskeleton organization; and neuron projection morphogenesis. Located in several cellular components, including microtubule cytoskeleton; nuclear lumen; and perinuclear region of cytoplasm. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

MAP8; BPY2IP1; C19orf5; VCY2IP1; VCY2IP-1;

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Detailed Information

Microtubule-associated protein 1S (MAP1S), formerly known as Chromosome 19 Open Reading Framework 5 (C19ORF5), was first discovered and named in 2005 and is a member of the microtubule-associated protein 1 (MAP1) family, widely distributed in human and mammalian cells. MAP1S not only regulates the process of cell mitosis, but also participates in the regulation of autophagy activity. As a member of the MAP1 family, MAP1S shares homology with other members of the MAP1 family, MAP1A and MAP1B, and regulates tubulin. MAP1S contains 3 MAP1's iconic domains with few additional sequences. Unlike MAP1A and MAP1B, MAP1S exists not only in the nervous system, but also in other organs such as the liver, spleen, and heart, and functions differently in different cells.

Figure 1. Chemical genetic identification of physiological CDKL5 substrates EB2 and MAP1S reveals its role as a regulator of neuronal microtubule dynamics. (Lucas L Baltussen, et al. 2018)

Biological Function of MAP1S

The study found that MAP1S, the first spindle protein found in large-scale screening, is associated with spindles in human and mammalian cells. MAP1S is localized to the central portion of the spindle microtubule assembly through the NH2 terminus to maintain microtubule-associated function during the cell division cycle. MAP1S has an indispensable regulation of the mitotic cycle, which is essential for maintaining cell proliferation and stability. MAP1S is an adaptor protein that acts on autophagy and can positively regulate autophagy activity and participate in the production and degradation of autophagosomes.

Relationship Between MAP1S and Tumorigenesis

MAP1S can affect gene instability and tumorigenesis by regulating autophagy. Autophagy dysfunction is closely related to tumorigenesis. Autophagy dysfunction induces oxidative stress, thereby attenuating mitotic checkpoints, causing DNA double helix cleavage, ultimately leading to genetic instability, which is the origin of most solid tumors. The study found that there is an important association between MAP1S-enhanced autophagy and oxidative stress and genetic instability.

Both high level of oxidative stress and gene instability can enhance the expression of MAP1S, which can activate autophagy and remove p62-related polymers and loss of functional organelles, thereby inhibiting the oxidative stress process, reducing the cleavage of DNA double helix and inhibiting gene instability. Because of this feedback loop, the body can maintain a balanced and stable development. Once MAP1S expression is lacking, autophagy activity will be affected, feedback loops will be broken, and genetic instability will increase. Therefore, the relationship between the enhanced autophagy of MAP1S and the instability of the suppressor gene and tumorigenesis is established.

The researchers found that MAP1S mutations are closely related to poor prognosis in patients with ovarian cancer. In a mouse model of hepatocellular carcinoma mediated by chemical tumorigenic factor (diethylnitrosamine), MAP1S regulates autophagy activity in tumors, while the mice deprived of MAP1S showed lower autophagy function, higher defective double-stranded DNA content and increased genetic instability than the normal control group, showing higher levels of genetic instability, increased incidence of hepatocellular carcinoma and higher malignancy. Studies have also shown that the protein expression levels of MAP1S and LRPPRC can be used as important indicators to judge the prognosis of patients with prostate cancer. In prostate cancer patients, MAP1S is mainly expressed in the cytoplasm of stratified epithelial cells. As the cancer cells proliferate, the number of MAP1S-expressing cells increases, and the intensity of MAP1S increases.

References:

Jiang X, Zhong W, Huang H, et al. (2015)Autophagy defects suggested by low levels of autophagy activator map1s and high levels of autophagy inhibitor lrpprc predict poor prognosis of prostate cancer patients. Molecular Carcinogenesis, 54(10), 1194-1204.
Li W, Zou J, Yue F, et al. (2016)Defects in MAP1S‐mediated autophagy cause reduction in mouse lifespans especially when fibronectin is overexpressed. Aging Cell 15.2:370-379.
Lucas L Baltussen, Priscilla D Negraes, Margaus Silverstre, et al. (2018)Chemical genetic identification of CDKL5 substrates reveals its role in neuronal microtubule dynamics. The EMBO Journal. (2018) e99763.

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