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FLASH GENE

Symbol

STK38

contributors: mct - updated : 31-05-2014

HGNC name	serine/threonine kinase 38
HGNC id	17847

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

EXPRESSION

Type	ubiquitous

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Digestive mouth tongue     highly   stomach       highly Lymphoid/Immune spleen       highly   thymus       highly Reproductive female system uterus     highly Urinary bladder       highly

tissue

System Tissue Tissue level 1 Tissue level 2 Level Pubmed Species Stage Rna symbol Connective bone

cells

System Cell Pubmed Species Stage Rna symbol Blood/Hematopoietic leukocyte

cell lineage
cell lines
fluid/secretion	blood

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	twelve protein kinase catalytic subdomains
	a potential bipartite nuclear localization signal

conjugated

PhosphoP

HOMOLOGY

interspecies	ortholog to murine Stk38
	homolog to Drosophila trc
	homolog to C. elegans sax-1
	ortholog to xenopus trc-prov1

Homologene

FAMILY	protein kinase superfamily
	nuclear-Dbf2-related (NDR) family of Ser/Thr kinases

CATEGORY

enzyme

SUBCELLULAR LOCALIZATION	intracellular
	intracellular,cytoplasm
	intracellular,nucleus
text	low levels present in the cytoplasm

basic FUNCTION	protein amino acid phosphorylation
	protein kinase cascade
	implicated in cell proliferation and/or tumor progression
	might play a role in the HIV-1 life cycle
	with STK38L, are proapoptotic kinases and key members of the RASSF1/STK4 signaling cascade
	required for accurate chromosome alignment at metaphase
	its kinase activity increased in early mitotic phase and was dependent on FRY and STK3
	STK38/STK38L have been implicated in controlling centrosome duplication and mitotic chromosome alignment downstream of the HIPPO kinase homologs MST1 and STK3
	its activation is required to prevent cell death in response to oxidative stress
	implicated to function in centrosome duplication, control of cell cycle and apoptosis
	novel role of STK38 in NFKB activation

CELLULAR PROCESS	cell life, proliferation/growth

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

a component

STK24-STK38/STK38L-CDKN1A axis is an important regulator of G(1)/S progression of mammalian cells

INTERACTION

DNA

RNA

small molecule	metal binding, cofactor, nucleotide,
	ATP
	Mg2+

protein	MOBKL1B
	homodimeric S100B
	HCCA2 and STK38L (this association dramatically stimulates STK38 and STK38L catalytic activity)
	MOBKL1A
	STK24-STK38-CDKN1A axis is an important regulator of G(1)/S progression of mammalian cells
	MICAL1 is a binding partner of NDR (nuclear Dbf2-related) kinases, STK4, and STK38
	regulates MYC protein stability and turnover in a kinase activity-dependent manner
	novel function of CCND1 in promoting cell cycle progression by enhancing STK38/STK38L kinase activity independent of CDK4
	STK38-mediated phosphorylation of CDC25A at Ser-76 and the subsequent degradation of CDC25A are required to promote DNA damage-induced G2/M checkpoint activation

cell & other

REGULATION

activated by	binding of S100B
	the binding of MOB1/MOBKL1A and MOB2/HCCA2 to the N-terminal of STK38 (autoinhibition released)

inhibited by	MOB2(negatively regulated by increased MOB2 expression)
	GSK3B, that inhibits STK38 full activation

Other

STK3-, FRY-, and MOB2-mediated activation of STK38 is crucial for the fidelity of mitotic chromosome alignment in mammalian cells

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function constitutional     --over   resulted in centrosome overduplication in a kinase-activity-dependent manner, while expression of kinase-dead STK38/STK38L or depletion of STK38/STK38L by small interfering RNA (siRNA) negatively affected centrosome duplication

Susceptibility

Variant & Polymorphism

Candidate gene
Marker
Therapy target
	System Type Disorder Pubmed cancer hemopathy   STK38 kinase inactivation abrogates apoptosis following B-cell receptor activation, whereas its silencing significantly decreases MYC levels and increases apoptosis, thus providing a novel viable target for treating B-cell lymphomas

ANIMAL & CELL MODELS