Entry - *609282 - MOB KINASE ACTIVATOR 1B; MOB1B - OMIM

 
 
* 609282

MOB KINASE ACTIVATOR 1B; MOB1B


Alternative titles; symbols

MOB1-LIKE PROTEIN 1A; MOBKL1A
MATS, DROSOPHILA, HOMOLOG OF, 2; MATS2


HGNC Approved Gene Symbol: MOB1B

Cytogenetic location: 4q13.3   Genomic coordinates (GRCh38) : 4:70,901,851-70,988,168 (from NCBI)


TEXT

▼ Cloning and Expression

Lai et al. (2005) identified a Drosophila protein belonging to the Mob1 superfamily that they termed Mats (Mob as tumor suppressor). By database analysis, they identified 2 human orthologs, MOBKL1B (609281) and MOBKL1A, which they named MATS1 and MATS2, respectively. The MATS2 protein contains 216 amino acids and shares 88% identity with Drosophila Mats.


▼ Gene Function

Lai et al. (2005) described the growth inhibitory functions of Drosophila Mats. Loss of Mats function resulted in increased cell proliferation, defective apoptosis, and induction of tissue overgrowth. Mats physically associated with Lats/Wts kinase (LATS1; 603473) and stimulated its catalytic activity.


▼ Mapping

Gross (2021) mapped the MOB1B gene to chromosome 4q13.3 based on an alignment of the MOB1B sequence (GenBank BC038112) with the genomic sequence (GRCh38).

▼ REFERENCES

  1. Gross, M. B. Personal Communication. Baltimore, Md. 8/17/2021.

  2. Lai, Z.-C., Wei, X., Shimizu, T., Ramos, E., Rohrbaugh, M., Nikolaidis, N., Ho, L.-L., Li, Y. Control of cell proliferation and apoptosis by Mob as tumor suppressor, Mats. Cell 120: 675-685, 2005. [PubMed: 15766530, related citations] [Full Text]


Contributors:
Matthew B. Gross - updated : 08/17/2021
Creation Date:
Stylianos E. Antonarakis : 3/29/2005
Edit History:
mgross : 08/17/2021
mgross : 03/29/2005

* 609282

MOB KINASE ACTIVATOR 1B; MOB1B


Alternative titles; symbols

MOB1-LIKE PROTEIN 1A; MOBKL1A
MATS, DROSOPHILA, HOMOLOG OF, 2; MATS2


HGNC Approved Gene Symbol: MOB1B

Cytogenetic location: 4q13.3   Genomic coordinates (GRCh38) : 4:70,901,851-70,988,168 (from NCBI)


TEXT

Cloning and Expression

Lai et al. (2005) identified a Drosophila protein belonging to the Mob1 superfamily that they termed Mats (Mob as tumor suppressor). By database analysis, they identified 2 human orthologs, MOBKL1B (609281) and MOBKL1A, which they named MATS1 and MATS2, respectively. The MATS2 protein contains 216 amino acids and shares 88% identity with Drosophila Mats.


Gene Function

Lai et al. (2005) described the growth inhibitory functions of Drosophila Mats. Loss of Mats function resulted in increased cell proliferation, defective apoptosis, and induction of tissue overgrowth. Mats physically associated with Lats/Wts kinase (LATS1; 603473) and stimulated its catalytic activity.


Mapping

Gross (2021) mapped the MOB1B gene to chromosome 4q13.3 based on an alignment of the MOB1B sequence (GenBank BC038112) with the genomic sequence (GRCh38).

REFERENCES

  1. Gross, M. B. Personal Communication. Baltimore, Md. 8/17/2021.

  2. Lai, Z.-C., Wei, X., Shimizu, T., Ramos, E., Rohrbaugh, M., Nikolaidis, N., Ho, L.-L., Li, Y. Control of cell proliferation and apoptosis by Mob as tumor suppressor, Mats. Cell 120: 675-685, 2005. [PubMed: 15766530] [Full Text: https://doi.org/10.1016/j.cell.2004.12.036]


Contributors:
Matthew B. Gross - updated : 08/17/2021

Creation Date:
Stylianos E. Antonarakis : 3/29/2005

Edit History:
mgross : 08/17/2021
mgross : 03/29/2005



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OMIM® and Online Mendelian Inheritance in Man® are registered trademarks of the Johns Hopkins University.
Copyright® 1966-2024 Johns Hopkins University.

NOTE: OMIM is intended for use primarily by physicians and other professionals concerned with genetic disorders, by genetics researchers, and by advanced students in science and medicine. While the OMIM database is open to the public, users seeking information about a personal medical or genetic condition are urged to consult with a qualified physician for diagnosis and for answers to personal questions.
OMIM® and Online Mendelian Inheritance in Man® are registered trademarks of the Johns Hopkins University.
Copyright® 1966-2024 Johns Hopkins University.
Printed: Nov. 16, 2024