Biomedical subjects

L Ling

Publications and source records attributed to L Ling.

At least 19 recordsLinked to original sources

PubMed2000

MIP-T3, a novel protein linking tumor necrosis factor receptor-associated factor 3 to the microtubule network.

In this study, we report the identification of a novel tumor necrosis factor receptor-associated factor 3 (TRAF3)-interacting protein designated MIP-T3. MIP-T3 is a 83-kDa protein with no significant homology to known mammalian proteins. MIP-T3 mRNA and TRAF3 mRNA are ubiquitously expressed, and TRAF3 is the only TRAF protein to interact with MIP-T3. The MIP-T3-TRAF3 interaction requires the coiled-coil TRAF-N domain of TRAF3. To our knowledge, this is the first case of a TRAF-binding protein that interacts with a single member of the TRAF family specifically through a TRAF-N coiled-coil domain. MIP-T3 binds to Taxol-stabilized microtubules and to tubulin in vitro, and MIP-T3 recruits TRAF3 to microtubules when both proteins are overexpressed in HeLa cells. In a 293 cell line stably expressing CD40, TRAF3 is released from the TRAF3.MIP-T3 complex and recruited to the CD40 receptor upon CD40 ligand stimulation. MIP-T3 may provide a novel mechanism in sequestering TRAF3 to the cytoskeletal network.

Amino Acid Sequence↗

PubMed2000

Regular articles: conditional disruption of hedgehog signaling pathway defines its critical role in hair development and regeneration.

Members of the vertebrate hedgehog family (Sonic, Indian, and Desert) have been shown to be essential for the development of various organ systems, including neural, somite, limb, skeletal, and for male gonad morphogenesis. Sonic hedgehog and its cognate receptor Patched are expressed in the epithelial and/or mesenchymal cell components of the hair follicle. Recent studies have demonstrated an essential role for this pathway in hair development in the skin of Sonic hedgehog null embryos. We have further explored the role of the hedgehog pathway using anti-hedgehog blocking monoclonal antibodies to treat pregnant mice at different stages of gestation and have generated viable offspring that lack body coat hair. Histologic analysis revealed the presence of ectodermal placode and primodium of dermal papilla in these mice, yet the subsequent hair shaft formation was inhibited. In contrast, the vibrissae (whisker) development appears to be unaffected upon anti-hedgehog blocking monoclonal antibody treatment. Strikingly, inhibition of body coat hair morphogenesis also was observed in mice treated postnatally with anti-hedgehog monoclonal antibody during the growing (anagen) phase of the hair cycle. The hairless phenotype was reversible upon suspension of monoclonal antibody treatment. Taken together, our results underscore a direct role of the Sonic hedgehog signaling pathway in embryonic hair follicle development as well as in subsequent hair cycles in young and adult mice. Our system of generating an inducible and reversible hairless phenotype by anti-hedgehog monoclonal antibody treatment will be valuable for studying the regulation and mechanism of hair regeneration.

Animals↗

PubMed1999

Action of the brain stem saccade generator during horizontal gaze shifts. I. Discharge patterns of omnidirectional pause neurons.

Omnidirectional pause neurons (OPNs) pause for the duration of a saccade in all directions because they are part of the neural mechanism that controls saccade duration. In the natural situation, however, large saccades are accompanied by head movements to produce rapid gaze shifts. To determine whether OPNs are part of the mechanism that controls the whole gaze shift rather than the eye saccade alone, we monitored the activity of 44 OPNs that paused for rightward and leftward gaze shifts but otherwise discharged at relatively constant average rates. Pause duration was well correlated with the duration of either eye or gaze movement but poorly correlated with the duration of head movement. The time of pause onset was aligned tightly with the onset of either eye or gaze movement but only loosely aligned with the onset of head movement. These data suggest that the OPN pause does not encode the duration of head movement. Further, the end of the OPN pause was often better aligned with the end of the eye movement than with the end of the gaze movement for individual gaze shifts. For most gaze shifts, the eye component ended with an immediate counterrotation owing to the vestibuloocular reflex (VOR), and gaze ended at variable times thereafter. In those gaze shifts where eye counterrotation was delayed, the end of the pause also was delayed. Taken together, these data suggest that the end of the pause influences the onset of eye counterrotation, not the end of the gaze shift. We suggest that OPN neurons act to control only that portion of the gaze movement that is commanded by the eye burst generator. This command is expressed by driving the saccadic eye movement directly and also by suppressing VOR eye counterrotation. Because gaze end is less well correlated with pause end and often occurs well after counterrotation onset, we conclude that elements of the burst generator typically are not active till gaze end, and that gaze end is determined by another mechanism independent of the OPNs.

Animals↗

PubMed1999

Short- and long-term consequences of canal plugging on gaze shifts in the rhesus monkey. I. Effects on gaze stabilization.

Short- and long-term consequences of canal plugging on gaze shifts in the rhesus monkey. I. Effects on gaze stabilization. To study the contribution of the vestibular system to the coordinated eye and head movements of a gaze shift, we plugged the lumens of just the horizontal (n = 2) or all six semicircular canals (n = 1) in monkeys trained to make horizontal head-unrestrained gaze shifts to visual targets. After the initial eye saccade of a gaze shift, normal monkeys exhibit a compensatory eye counterrotation that stabilizes gaze as the head movement continues. This counterrotation, which has a gain (eye velocity/head velocity) near one has been attributed to the vestibuloocular reflex (VOR). One day after horizontal canal plugging, the gain of the passive horizontal VOR at frequencies between 0.1 and 1.0 Hz was <0.10 in the horizontal-canal-plugged animals and zero in the all-canal-plugged animal. One day after surgery, counterrotation gain was approximately 0.3 in the animals with horizontal canals plugged and absent in the animal with all canals plugged. As the time after plugging increased, so too did counterrotation gain. In all three animals, counterrotation gain recovered to between 0.56 and 0.75 within 80-100 days. The initial loss of compensatory counterrotation after plugging resulted in a gaze shift that ended long after the eye saccade and just before the end of the head movement. With recovery, the length of time between the end of the eye saccade and the end of the gaze movement decreased. This shortening of the duration of reduced gain counterrotation occurred both because head movements ended sooner and counterrotation gain returned to 1.0 more rapidly relative to the end of the eye saccade. Eye counterrotation was not due to activation of pursuit eye movements as it persisted when gaze shifts were executed to extinguished targets. Also counterrotation was not due simply to activation of neck receptors because counterrotation persisted after head movements were arrested in midflight. We suggest that the neural signal that is used to cause counterrotation in the absence of vestibular input is an internal copy of the intended head movement.

Animals↗

PubMed1999

Apparent dissociation between saccadic eye movements and the firing patterns of premotor neurons and motoneurons.

Saccadic eye movements result from high-frequency bursts of activity in ocular motoneurons. This phasic activity originates in premotor burst neurons. When the head is restrained, the number of action potentials in the bursts of burst neurons and motoneurons increases linearly with eye movement amplitude. However, when the head is unrestrained, the number of action potentials now increase as a function of the change in the direction of the line of sight during eye movements of relatively similar amplitudes. These data suggest an apparent uncoupling of premotor neuron and motoneuron activity from the resultant eye movement.

Abducens Nerve↗

PubMed1999

Academic emergency medicine's future. The SAEM Task Force on Emergency Medicine's Future. Society for Academic Emergency Medicine.

Emergency medicine (EM) will change over the next 20 years more than any other specialty. Its proximity to and interrelationships with the community, nearly all other clinicians (physicians and nonphysicians), and scientific/technologic developments guarantee this. While emergency physicians (EPs) will continue to treat both emergent and nonemergent patients, over the next decades our interventions, methods, and place in the medical care system will probably become unrecognizable from the EM we now practice and deliver. This paper, developed by the Society for Academic Emergency Medicine (SAEM) Task Force on Academic Emergency Medicine's Future, was designed to promote discussions about and actions to optimize our specialty's future. After briefly discussing the importance of futures planning, it suggests "best-case," "worst-case," and most probable future courses for academic EM over the next decades. The authors predict that EPs will practice a much more technologic and accurate form of medicine, with diagnostic, patient, reference, and consultant information rapidly available to them. They will be at the center of an extensive consultation network stemming from major medical centers and the purveyors of a sophisticated home health system, very similar to or even more advanced than what is now delivered on hospital wards. The key to planning for our specialty is for EM organizations, academic centers, and individuals to act now to optimize our possible future.

Academic Medical Centers↗

PubMed1999

Reconstruction plates to bridge mandibular defects: a clinical and experimental investigation in biomechanical aspects.

A retrospective study of 68 patients was carried out to assess the complications arising from the use of reconstruction plates in the maintainance of space and contour following mandibular segmental resection. Skin or mucosal perforation, plate fracture and loss of screw retention were the main complications. The most susceptible sites to screw loosening in the plates were situated nearest to and farthest from the resection margin on the proximal residual segments. Some of the possible causative biomechanical mechanisms of plate failure were studied using photoelastic models simulating the types of mandibular defect and plate fixation. Isochromatic fringe analysis was used to analyse stress lines in the bone surrounding screws. It was found that, during functional loading, moment and shear forces produced high concentrations of squeeze and press stress in this bone, causing bone resorption with consequent loss of screw retention.

Birefringence↗

PubMed1998

Slow recovery of impaired phrenic responses to hypoxia following perinatal hyperoxia in rats.

1. Previous studies demonstrated that both ventilatory and phrenic nerve responses to acute hypoxia are greatly attenuated in adult rats (3-5 months old) previously exposed to 1 month of perinatal hyperoxia (60 % O2; perinatal treated rats). The present study tested the hypothesis that this functional impairment recovers spontaneously with advancing age in perinatal treated rats. 2. Hypoxia-induced chemoreflexes were examined by measuring integrated phrenic responses to strictly controlled isocapnic hypoxia in urethane-anaesthetized, vagotomized, paralysed and ventilated rats at different ages. 3. At 50 mmHg Pa,O2 (arterial O2 partial pressure), the hypoxia-induced increase in minute phrenic activity was significantly attenuated in both 3- to 5-month-old (166 +/- 15% of baseline) and 6-month-old (130 +/- 17%) perinatal treated rats, relative to 3- to 6-month-old, untreated control rats (279 +/- 28%; both P < 0.05). However, at 40 mmHg Pa,O2, the hypoxic minute phrenic activity response was attenuated only in 3- to 5-month-old (154 +/- 33%), but not 6-month-old (232 +/- 33%) perinatal treated rats versus control rats (293 +/- 30%). 4. The minute phrenic activity response to hypoxia was not significantly different between geriatric perinatal treated rats (14-15 months) and untreated geriatric control rats at either 50 mmHg (treated: 250 +/- 20% versus control: 274 +/- 23%) or 40 mmHg Pa,O2 (treated: 292 +/- 19% versus control: 315 +/- 36%). 5. These data suggest that partial spontaneous recovery may occur in 6-month-old perinatal treated rats and that full recovery occurs by 15 months of age.

Animals↗

PubMed1998

Chemoafferent degeneration and carotid body hypoplasia following chronic hyperoxia in newborn rats.

1. To define the role of environmental oxygen in regulating postnatal maturation of the carotid body afferent pathway, light and electron microscopic methods were used to compare chemoafferent neurone survival and carotid body development in newborn rats reared from birth in normoxia (21 % O2) or chronic hyperoxia (60 % O2). 2. Four weeks of chronic hyperoxia resulted in a significant 41 % decrease in the number of unmyelinated axons in the carotid sinus nerve, compared with age-matched normoxic controls. In contrast, the number of myelinated axons was unaffected by hyperoxic exposure. 3. Chemoafferent neurones, located in the glossopharyngeal petrosal ganglion, already exhibited degenerative changes following 1 week of hyperoxia from birth, indicating that even a relatively short hyperoxic exposure was sufficient to derange normal chemoafferent development. In contrast, no such changes were observed in the vagal nodose ganglion, demonstrating that the effect of high oxygen levels was specific to sensory neurones in the carotid body afferent pathway. Moreover, petrosal ganglion neurones were sensitive to hyperoxic exposure only during the early postnatal period. 4. Chemoafferent degeneration in chronically hyperoxic animals was accompanied by marked hypoplasia of the carotid body. In view of previous findings from our laboratory that chemoafferent neurones require trophic support from the carotid body for survival after birth, we propose that chemoafferent degeneration following chronic hyperoxia is due specifically to the loss of target tissue in the carotid body.

Afferent Pathways↗

PubMed1998

NF-kappaB-inducing kinase activates IKK-alpha by phosphorylation of Ser-176.

Activation of the transcription factor NF-kappaB by inflammatory cytokines involves the successive action of NF-kappaB-inducing kinase (NIK) and two IkappaB kinases, IKK-alpha and IKK-beta. Here we show that NIK preferentially phosphorylates IKK-alpha over IKK-beta, leading to the activation of IKK-alpha kinase activity. This phosphorylation of IKK-alpha occurs specifically on Ser-176 in the activation loop between kinase subdomains VII and VIII. A mutant form of IKK-alpha containing alanine at residue 176 cannot be phosphorylated or activated by NIK and acts as a dominant negative inhibitor of interleukin 1- and tumor necrosis factor-induced NF-kappaB activation. Conversely, a mutant form of IKK-alpha containing glutamic acid at residue 176 is constitutively active. Thus, the phosphorylation of IKK-alpha on Ser-176 by NIK may be required for cytokine-mediated NF-kappaB activation.

Amino Acid Sequence↗

PubMed1997

Fibronectin type III repeats mediate RGD-independent adhesion and signaling through activated beta1 integrins.

Many cell-surface and extracellular matrix proteins contain multiple modular domains known as fibronectin type III (FNIII) repeats. Cells adhere to the extracellular matrix proteins fibronectin and tenascin in part by the interaction of certain integrins with the Arg-Gly-Asp (RGD) sequence, displayed on specific FNIII repeats. We have found that, after experimental activation of beta1 integrins, a number of cell types adhere and spread on FNIII repeats lacking RGD, derived from extracellular matrix proteins and cytokine receptors. Interaction between individual FNIII domains and beta1 integrins mediates focal adhesion kinase phosphorylation and subsequent stress fiber and focal contact formation. These data suggest that many FNIII-containing proteins may bind and signal through activated beta1 integrins, dramatically expanding the potential for integrin-dependent intercellular and cell-matrix communication.

Animals↗

PubMed1997

The amino-terminal region of Tyk2 sustains the level of interferon alpha receptor 1, a component of the interferon alpha/beta receptor.

Tyk2 belongs to the Janus kinase (JAK) family of receptor associated tyrosine kinases, characterized by a large N-terminal region, a kinase-like domain and a tyrosine kinase domain. It was previously shown that Tyk2 contributes to interferon-alpha (IFN-alpha) signaling not only catalytically, but also as an essential intracellular component of the receptor complex, being required for high affinity binding of IFN-alpha. For this function the tyrosine kinase domain was found to be dispensable. Here, it is shown that mutant cells lacking Tyk2 have significantly reduced IFN-alpha receptor 1 (IFNAR1) protein level, whereas the mRNA level is unaltered. Expression of the N-terminal region of Tyk2 in these cells reconstituted wild-type IFNAR1 level, but did not restore the binding activity of the receptor. Studies of mutant Tyk2 forms deleted at the N terminus indicated that the integrity of the N-terminal region is required to sustain IFNAR1. These studies also showed that the N-terminal region does not directly modulate the basal autophosphorylation activity of Tyk2, but it is required for efficient in vitro IFNAR1 phosphorylation and for rendering the enzyme activatable by IFN-alpha. Overall, these results indicate that distinct Tyk2 domains provide different functions to the receptor complex: the N-terminal region sustains IFNAR1 level, whereas the kinase-like domain provides a function toward high affinity ligand binding.

Cell Line↗

PubMed1997

Integrated phrenic responses to carotid afferent stimulation in adult rats following perinatal hyperoxia.

1. Hypoxic ventilatory responses are greatly attenuated in adult rats exposed to moderate hyperoxia (60% O2) during the first month of life (perinatal treated rats). The present study was designed to test the hypothesis that perinatal hyperoxia impairs central integration of carotid chemoreceptor afferent inputs, thereby diminishing the hypoxic ventilatory response. 2. Time-dependent phrenic nerve responses to electrical stimulation of the carotid sinus nerve (CSN) and steady-state relationships between CSN stimulation frequency and phrenic nerve output were compared in control and perinatal treated rats. The rats were urethane anaesthetized, vagotomized, paralysed and artificially ventilated. End-tidal CO2 was monitored and maintained at isocapnic levels; arterial blood gases were determined. 3. Two stimulation protocols were used: (1) three 2 min episodes of CSN stimulation (20 Hz, 0.2 ms duration, 3 x threshold), separated by 5 min intervals; and (2) nine 45 s episodes of CSN stimulation with stimulus frequencies ranging from 0.5 to 20 Hz (0.2 ms duration, 3 x threshold), separated by 4 min intervals. 4. The mean threshold currents to elicit phrenic responses were similar between groups. Burst frequency (f, burst min-1), peak amplitude of integrated phrenic activity (integral of Phr), and minute phrenic activity (integral of Phr x f) during and after CSN stimulation were not distinguishable between groups in either protocol at any time or at any stimulus intensity (P > 0.05). 5. Perinatal hyperoxia does not alter temporal or steady-state phrenic responses to CSN stimulation, suggesting that the central integration of carotid chemoreceptor afferent inputs is not impaired in perinatal treated rats. It is speculated that carotid chemoreceptors per se are impaired in perinatal treated rats.

Animals↗

PubMed1997

Phrenic responses to isocapnic hypoxia in adult rats following perinatal hyperoxia.

The purpose of this study was to test the hypothesis that carotid body-mediated, phrenic nerve responses to hypoxia are attenuated in adult rats that had been previously exposed to perinatal hyperoxia (one month of 60% O2; perinatal treated rats.) Integrated phrenic nerve responses to strictly controlled isocapnic hypoxia were measured in urethane-anesthetized, vagotomized, paralyzed and ventilated adult rats 2-5 months after perinatal hyperoxia, before and after bilateral carotid denervation. In untreated control rats, phrenic burst frequency, peak amplitude of integrated phrenic activity and minute phrenic activity increased 21 +/- 3 bursts/min (mean +/- SE), 158 +/- 20% and 279 +/- 34%, respectively, during hypoxia (50 Torr PaO2). In contrast, phrenic nerve activity increased to a significantly lesser degree in perinatal treated rats (frequency, 12 +/- 2 bursts/min; amplitude, 87 +/- 13%; minute activity, 150 +/- 19%; all P < 0.05). Hypoxic phrenic responses were abolished by carotid degeneration in both rat groups. In rats exposed to hyperoxia as adults, hypoxic phrenic responses were not attenuated versus untreated control rats. The data indicate that carotid body-mediated, isocapnic hypoxic chemoreflexes are impaired in perinatal treated rats, an effect unique to development. These effects cannot be accounted for by differences in blood gases (O2 or CO2) or pulmonary mechanics.

Animals↗

PubMed1997

Developmental plasticity of the hypoxic ventilatory response.

This paper will describe recent studies concerning the existence of developmental plasticity in the hypoxic ventilatory control system and the locus of the functional impairment following perinatal sensory suppression. Suppression of peripheral arterial chemoreceptor activity was achieved by exposing rats to hyperoxia (60% O2) for the first month of life; all measurements were conducted 2-5 months after the exposure (perinatal treated rats). Hypoxic (but not hypercapnic) ventilatory responses were severely attenuated in awake perinatal treated rats, but not in rats exposed to hyperoxia as adults, indicating that the persistent effect is unique to development and is not the nonspecific result of O2 toxicity. Impairments of the hypoxic ventilatory response due to changes in pulmonary mechanics, gas exchange or central integration of carotid chemoafferent inputs were all ruled out as primary causal factors. However, a persistent impairment of carotid chemotransduction in perinatal treated rats was apparent. These studies suggest that the hypoxic ventilatory response is susceptible to developmental plasticity, and that a carotid chemoreceptor deficit is the primary cause. These findings may have important clinical implications for patients subjected to excessive O2 therapy during neonatal intensive care.

Animals↗

PubMed1997

Gain adaptation of eye and head movement components of simian gaze shifts.

Gain adaptation of eye and head movement components of simian gaze shifts. J. Neurophysiol. 78: 2817-2821, 1997. To investigate the site of gaze adaptation in primates, we reduced the gain of large head-restrained gaze shifts made to 50 degrees target steps by jumping the target 40% backwards during a targeting saccade and then tested gain transfer to the eye- and head-movement components of head-unrestrained gaze shifts. After several hundred backstep trials, saccadic gain decreased by at least 10% in 8 of 13 experiments, which were then selected for further study. The minimum saccadic gain decrease in these eight experiments was 12.8% (mean = 18.4%). Head-unrestrained gaze shifts to ordinary 50 degrees target steps experienced a gain reduction of at least 9.3% (mean = 14.9%), a mean gain transfer of 81%. Both the eye and head components of the gaze shift also decreased. However, average head movement gain decreased much more (22.1%) than eye movement gain (9.2%). Also, peak head velocity generally decreased significantly (20%), but peak eye velocity either increased or remained constant (average increase of 5.6%). However, the adapted peak eye and head velocities were appropriate for the adapted, smaller gaze amplitudes. Similar dissociations in eye and head metrics occurred when head-unrestrained gaze shifts were adapted directly (n = 2). These results indicated that head-restrained saccadic gain adaptation did not produce adaptation of eye movement alone. Nor did it produce a proportional gain change in both eye and head movement. Rather, normal eye and head amplitude and velocity relations for a given gaze amplitude were preserved. Such a result could be explained most easily if head-restrained adaptation were realized before the eye and head commands had been individualized. Therefore, gaze adaptation is most likely to occur upstream of the creation of separate eye and head movement commands.

Acclimatization↗

PubMed1996

Attenuation of the hypoxic ventilatory response in adult rats following one month of perinatal hyperoxia.

1. This study was designed to test the hypothesis that perinatal suppression of peripheral arterial chemoreceptor inputs attenuates the hypoxic ventilatory response in adult rats. Perinatal suppression of peripheral chemoreceptor activity was achieved by exposing rats to hyperoxia throughout the first month of life. 2. Late-gestation pregnant rats were housed in a 60% O2 environment, exposing the pups to hyperoxia from several days prior to birth until they were returned to normoxia on postnatal day 28. These perinatally treated rats were then reared to adulthood (3-5 months old) in normoxia. In addition to the mother rats, adult male rats were also exposed to hyperoxia, creating an adult-treated control group. Two to four months after the hyperoxic exposure, treated rats were compared with untreated male rats of similar age. 3. A whole-body, flow-through plethysmograph was used to measure hypoxic and hypercapnic ventilatory responses of the unanaesthetized adult rats. In moderate hypoxia (arterial oxygen partial pressure, Pa,O2 approximately 48 mmHg). VE (minute ventilation) and the ratio VE/VCO2 (ventilation relative to CO2 production) increased by 16.7 +/- 4.0 and 35.4 +/- 3.4%, respectively, in perinatal-treated rats (means +/- S.E.M.), but increased more in untreated control rats (51.4 +/- 2.8 and 83.1 +/- 4.3%; both P < 10(-6)). 4. In contrast to the impaired hypoxic ventilatory response, ventilatory responses to hypercapnia (5% CO2) were similar between untreated control and perinatal-treated rats. 5. Impaired hypoxic responsiveness was unique to the perinatal-treated rats since hypoxic ventilatory responses were not attenuated in adult-treated rats. 6. The results indicate that ventilatory responses to hypoxaemia are greatly attenuated in adult rats that had experienced hyperoxia during their first month of life, and suggest that normal hypoxic ventilatory control mechanisms are susceptible to developmental plasticity.

Animals↗

PubMed1996

Identification of the major autophosphorylation sites of Nyk/Mer, an NCAM-related receptor tyrosine kinase.

Nyk/Mer receptor tyrosine kinase is a new member of the Ufo/Axl tyrosine kinase family and is characterized by its neural cell adhesion molecule-like extracellular domain. By using a vaccinia virus expression system to express a constitutively activated form of Nyk, we identified the major sites of Nyk autophosphorylation in tryptic peptide IY749SGDY753Y754R. Tyr-749, Tyr-753, and Tyr-754 in this peptide lie in the activation loop of the kinase domain. We also studied a series of Nyk mutants in which the three tyrosine residues were replaced individually, in pairs, or all together by phenylalanine. Single mutations of Tyr-749 or Tyr-753 to phenylalanine reduced Nyk kinase activity toward exogenous substrate to 39 or 10% of that of the wild type Nyk, respectively, whereas the Tyr-754 mutant is completely inactive. All of the double and triple Tyr-Phe mutants reduced Nyk kinase activity to a level below the background. Similar results were obtained when Nyk autophosphorylation levels were examined. Our studies suggest that full activity of Nyk/Mer kinase requires phosphorylation of all three tyrosine residues in the kinase domain (Tyr-749, Tyr-753, and Tyr-754) and that Nyk kinase activity is modulated by the level of autophosphorylation in the kinase domain. Given the highly conserved nature of this region among the Ufo/Axl receptor family members, the information presented in this report may provide insight to the biochemical properties of other members of this family.

Amino Acid Sequence↗